Maine, USA. Nebraska, USA. Related events American Civil War. American Revolution. World War II. Johnstown Flood. Sinking of the Titanic. Spanish-American War. Helpers smithli , SimoneA , Avron 50 , lquilter 9 , justablondemoment 2 , abbottthomas 1 , NinieB 1 , JenniferRobb 1 , sqoozie 1 , leselotte 1 , jefbra 1 , Conkie 1. A Torch for Trinity by Colleen L. Restore the Joy by Sara Mitchell. Reflections of the Heart by Sally Laity. Candleshine by Colleen L. Desert Rose by Colleen L. Heartstrings by Irene B. Song of Laughter by Lauraine Snelling.
River of Fire by Jacquelyn Cook. Cottonwood Dreams by Norene Morris. Passage of the Heart by Kjersti Hoff Baez. Silence in the Sage by Colleen L. Llama Lady by VeraLee Wiggins. Shores of Promise by Kate Blackwell. Indy Girl by Brenda Bancroft. Gone West by Kathleen Karr. Whispers in the Wilderness by Colleen L.
Rebar by Mary Carpenter Reid. Mountain House by Mary Louise Colln. Beyond the Searching River by Jacquelyn Cook. From The Heart by Sara Mitchell. Dream Spinner by Sally Laity. The Promised Land by Kathleen Karr. Sweet Shelter by VeraLee Wiggins. When Comes the Dawn by Brenda Bancroft. Drums of Shelomoh by Yvonne Lehman.
Rainbow Harvest by Norene Morris.
Perfect Love by Janelle Jamison. Search for Tomorrow by Mary Hawkins. Veiled Joy by Colleen L. Dakota Dream by Lauraine Snelling. Tender Journeys by Janelle Jamison. Shores of Deliverance by Kate Blackwell. Yesterday's Tomorrows by Linda Herring. Dance in the Distance by Kjersti Hoff Baez. Tapestry of Tamar by Colleen L. Midnight Music by Janelle Burnham Schneider. Treasure of the Heart by JoAnn A. A Light in the Window by Janelle Jamison.
Free to Love by Doris English. More Than Conquerors by Kay Cornelius. Picture Perfect by Susan Kirby. The Willing Heart by Janelle Jamison. Crows' Nests and Mirrors by Colleen L. Angel Face by Frances Carfi Matranga. Autumn Love by Ann Bell. Dakota Dusk by Lauraine Snelling. Rivers Rushing to the Sea by Jacquelyn Cook.
Between love and loyalty Hearstong Presents by Susannah Hayden. A New Song by Kathleen Yapp. Destiny's Road by Janelle Jamison. Song of Captivity by Linda Herring. Music in the Mountains by Colleen L. Heartbreak Trail by VeraLee Wiggins. An Unwilling Warrior by Andrea Shaar. Proper Intentions by Dianne Christner. Southern Gentleman by Yvonne Lehman. Heart's Desire by Paige Winship Dooly. Lamp In Darkness by Connie Loraine. Pocketful of Love by Loree Lough. Contagious Love by Ann Bell. Cater to a Whim by Norma Jean Lutz.
Sign of the Eagle by Kay Cornelius. Iditarod Dream by Janelle Jamison. To Be Strong by Carolyn Scheidies. Sign of the Dove by Kay Cornelius. Flower of Seattle by Colleen L. Beauty for Ashes by Becky Melby. River of Peace by Janelle Burnham. If Given a Choice by Tracie J. Circle of Love by Alma Blair. Ragdoll Heartsong Presents by Kelly R. Pioneer Legacy by Norene Morris. Lofty Ambitions by Dianne Christner. Inspired Love by Ann Bell. Callie's Mountain by Veda Boyd Jones. Captives of the Canyon by Colleen L. Between the Memory and the Moment by Susannah Hayden. The Quiet Heart by Rae Simons.
Farther Along the Road by Susannah Hayden. Flickering Flames by Connie Loraine. Love's Tender Gift by Elizabeth Murphy. Mountain Man by Yvonne Lehman. Misplaced Angel by VeraLee Wiggins. Search for Yesterday by Mary Hawkins. A Matter of Security by Kay Cornelius. Love in the Prairie Wilds by Robin Chandler.
Lost Creek Mission by Cheryl Tenbrook. The Road Home by Susannah Hayden. Sign of the Spirit by Kay Cornelius. Distant Love by Ann Bell. Angel's Cause by Tracie Peterson. Flying High by Phyllis Humphrey. Flower of the West by Colleen L. Mockingbird's Song by Janet Gortsema. Dancing in the Darkness by Janelle Burnham Schneider. Dreams of the Pioneers by Linda Herring. Follow The Leader by Loree Lough.
Belated Follower by Colleen L. Healing Love by Ann Bell. Tulsa Tempest by Norma Jean Lutz. Pocketful of Promises by Loree Lough. Flower of the North by Colleen L. To Keep Faith by Carolyn Scheidies. Montana Sky by Loree Lough. Alas my love by Tracie Peterson. Consider Her Ways by Fran Vincent. Priscilla Hires a Husband by Loree Lough. Garment of Praise by Becky Melby. Against That Day by Rae Simons. Tulsa Turning by Norma Jean Lutz.
The Hasty Heart by Helen Spears. James's Joy by Cara McCormack. Where There is Hope by Carolyn R. Nepali Noon by Susannah Hayden. Eagles for Anna by Catherine Runyon. Her Father's Love by Nancy Lavo. Friend of a Friend by Jill Richardson. Retreat to Love by Nancy N. Flower of Alaska by Colleen L. Uncertain Heart by Andrea Boeshaar. A Kindled Spark by Colleen L. Small Blessings by DeWanna Pace. From Ashes to Glory by Bonnie L. Compassionate Love by Ann Bell.
Wait for the Morning by Kjersti Hoff Baez. Dreams Fulfilled by Linda Herring. Eagle Pilot by Jill Stengl. Watercolor Castles by Ranee McCollum. Dakota December by Lauraine Snelling. If Only Heartsong Presents, No. Search for Today by Mary Hawkins. Ample Portions by Dianne Christner. Megan's Choice by Rosey Dow. Politically Correct by Kay Cornelius. The Eagle and the Lamb by Darlene Mindrup. Love's Tender Path by Birdie L. Crosswinds by Shirley Rohde. Tomorrow's Rainbow by VeraLee Wiggins. Tulsa Trespass by Norma Jean Lutz.
Black Hawk's Feather by Carolyn R. Odyssey of Love by Melanie Panagiotopoulos. Hawaiian Heartbeat by Yvonne Lehman. Song of the Dove by Peggy Darty. Thief of My Heart by Catherine Bach. Finally, Love by Jill Stengl. Edge of Destiny by Darlene Mindrup. Wings of the Dawn by Tracie J. Bridget's Bargain by Loree Lough.
Treasure of the Keys by Stephen A. Emma's Orphans by Loree Lough. Faith Came Late by Freda Chrisman. Glowing Embers by Colleen L. The Lady Rose by Joyce Williams. Valiant Heart by Sally Laity. The Neighbor by Debra White Smith. Annie's Song by Andrea Boeshaar. The Rising Son by Darlene Mindrup. Crossroads by Tracie Peterson. Brianna's Pardon by Gloria Clover.
Strong as the Redwood by Kristin Billerbeck. Something from Nothing by Nancy Lavo. Anna's Hope by Birdie L. The Refuge by Rae Simons. Kate Ties the Knot by Loree Lough. Tender Remembrance by Una McManus. The Alaskan Way by Marilou H. Heaven's Child by Gina Fields. The Starfire Quilt by Alice Allen. Hearth of Fire by Colleen L. What Love Remembers by Muncy G. For a Song by Kathleen Scarth. Walking the Dog by Gail Sattler. Promise Me Forever by Andrea Boeshaar. Where Leads the Heart by Colleen Coble.
Albert's Destiny by Birdie L. Summer Place by Peggy Darty. The Healing Promise by Hannah Alexander. Along Unfamiliar Paths by Ann Rognlie. The Wedding Wish by Loree Lough. In Lizzy's Image by Carolyn R. Texas Honor by Debra White Smith. Rich Blessings by Racine Leonard Davis. Sweet Surrender by JoAnn A. The Perfect Wife by Gina Fields. After the Storm by Yvonne Lehman. Rehoboth by DiAnn Mills. A Child of Promise by Jill Stengl. Tend the Light by Susannah Hayden.
One More Chance by Kimberley Comeaux. A Sense of Belonging by Terry Fowler. Em's Only Chance by Rosey Dow. Second Time Around by Andrea Boeshaar. Seasons by Gail Gaymer Martin. Maid of Honor by Carolyn R. Song of the Cimarron by Kelly R. Call of the Mountain by Yvonne Lehman. Piano Lessons by Gail Sattler. Silent Stranger by Peggy Darty. Prize Package by Catherine Runyon. The Reluctant Bride by Helen Spears. Out of the Darkness by Dianna Crawford.
Sealed with a Kiss by Loree Lough. Faith in the Great Southland by Mary Hawkins. Love Remembered by Ann Bell. Born for This Love by Brenda Bancroft. Hope in the Great Southland by Mary Hawkins. Fortress of Love by Melanie Panagiotopoulos. Country Charm by DiAnn Mills. Love in the Great Southland by Mary Hawkins. Gone Camping by Gail Sattler.
A Tender Melody by Birdie L. Stranger's Bride by Denise Hunter. Dreaming of Castles by Gail Gaymer Martin. Hidden Trails by Janelle Burnham Schneider. Behind The Mask by Lauralee Bliss. Escape by Kathleen Paul. Time for a Miracle by Jill Stengl. Drink from the Sky by Darlene Mindrup. Ozark Sunrise by Hannah Alexander. Somewhere a Rainbow by Yvonne Lehman. Birdsong Road by Mary Louise Colln. Texas Rose by Debra White Smith. Double Take by Terry Fowler.
Thanks to a Lonely Heart by Elaine Bonner. Wild Tiger Wind by Gayle Buck.
Race for the Roses by Lauraine Snelling. Courtin' Patience by Kimberley Comeaux. After the Flowers Fade by Amy Rognlie. Ice Castle by Joyce Livingston. Finding Courtney by Birdie L. Texas Lady by Debra White Smith. Whiter Than Snow by Yvonne Lehman. Undaunted Faith by Andrea Boeshaar. The Name Game by Muncy G. Stacy's Wedding by Aisha Ford. Rebellious Heart by Rachel Druten. Light Beckons the Dawn by Susannah Hayden. Still Waters by Gina Fields. Twin Victories by Cathy Marie Hake. Storm by Dianne Christner. Catch of a Lifetime by Yvonne Lehman. Frieda's Song by Kathleen Scarth.
Mark of Cain by Darlene Mindrup. Never a Bride by Denise Hunter.
Southern Sympathies by Andrea Boeshaar. Lisa's Broken Arrow by Rosey Dow. Texas Angel by Debra White Smith. Dance from the Heart by Louise Tucker Jones. Grant Me Mercy by Jill Stengl. Lessons in Love by Nancy Lavo. Familiar Strangers by Gina Fields. Love Abounds by Ann Bell. C for Victory by Joan Croston.
Healing Sarah's Heart by Tammy Shuttlesworth. Equestrian Charm by DiAnn Mills. A Time to Embrace by Lynn A. Susannah's Secret by Kimberley Comeaux. Castle in the Clouds by Andrea Boeshaar. Secret Ballot by Yvonne Lehman. At the Golden Gate by Freda Chrisman. The Wife Degree by Aisha Ford. Almost Twins Heartsong Presents, No. Sleigh Bells Heartsong Presents, No.
A Living Soul by Hannah Alexander. Spirit of the Eagle by Gina Fields. Remnant of Victory by Jeri Odell. The Sea Beckons by Birdie L. Sonoran Sunrise by Nancy J. Both Sides of the Easel by Barbara Youree. From Russia with Love by Colleen Coble. Yesteryear by Gloria Brandt. Captive Heart by Darlene Mindrup.
In the Secret Place by Pamela Griffin. Condo Mania by Muncy G. Darling Cassidy by Tracey V. Mustering Courage by Lynn A. To the Extreme by Tish Davis. Remnant of Grace by Susan K. An Unmasked Heart by Andrea Boeshaar. Love Ahoy by Colleen Coble. Myles from Anywhere by Jill Stengl. Tears in a Bottle by Gina Fields. A Few Flowers by Gail Sattler. Northern Exposure by Joyce Livingston.
Out in the Real World by Kathleen Paul. One with the Wind by Kelly R. The Stranger's Kiss by Yvonne Lehman. Cassidy's Charm by DiAnn Mills. Vision of Hope by Marilou H. Lizzy's Hope by Lynn A. The Prodigal's Welcome by Kristin Billerbeck. Viking Pride by Darlene Mindrup. Chastity's Angel by Linda Ford. An Ostrich a Day by Nancy J.
The Elusive Mr. Perfect by Tamela Hancock Murray. My Beloved Waits by Peggy Darty. Candy Cane Calaboose by Janet Spaeth. Remnant Of Light by Melanie Panagiotopoulos. Sweet Spring by Marilou H. Pride and Pumpernickel by Aisha Ford. Secrets Within by Gail Gaymer Martin. Crane's Bride by Linda Ford. Talking for Two by Wanda E.
Risa's Rainbow by Andrea Boeshaar. Hidden Treasures by Jeri Odell. Tarah's Lessons by Tracey V. Beacon of Truth by Pamela Griffin. Carolina Pride by Terry Fowler. Bittersweet Bride by Denise Hunter. Extreme Grace by Tish Davis. Sonoran Star by Nancy J. Unexpected Delivery by Cathy Marie Hake.
Hand Quilted with Love by Joyce Livingston. The Heart Knows by Elaine Bonner. Ring of Hope by Birdie L. Maggie's Mistake by Colleen Coble. Sonoran Sweetheart by Nancy J. An Unexpected Surprise by Rosey Dow. Mended Wheels by Ann Bell. Flames of Deceit by Rosey Dow.
Charade by Priscilla Humphrey. Great Southland Gold by Mary Hawkins. Whole in One by Alisha Ford. Sonoran Secret by Nancy J. Happily Ever After by Melanie Panagiotopoulos. Cords of Love by Lynn A. Trunk Of Surprises by Diann Hunt. Dark Side of the Sun by Rachel Druten. His Christmas Angel by Gail Sattler. Past the Ps Please by Yvonne Lehman. To Walk in Sunshine by Sally Laity. Precious Burdens by Cathy Marie Hake. Licorice Kisses by DiAnn Mills. Lucy's Quilt by Joyce Livingston.
The Neighborly Thing by Wanda E. Red River Bride by Colleen Coble. Be My Valentine by Joyce Livingston. Angel's Roost by Janet Spaeth. Raining Fire by Lynn A. Laney's Kiss by Tracey V. In Search of Love by Christine Lynxwiler. Precious Jewels by Nancy J. Lizzie Heartsong Presents, No.
Term of Love by Myrtlemay Pittman Crane. Viking Honor by Darlene Mindrup. Emily's Place by Tracey V. A Storybook Finish by Lauralee Bliss. Two Hearts Wait by Freda Chrisman. Double Exposure by Sally Laity. The Summer Girl by Andrea Boeshaar. Clowning Around by Wanda E. Cora by Mildred Colvin. Love is Patient by Cathy Marie Hake. Love is Kind by Joyce Livingston. Maryelle Heartsong Presents by Linda Ford. His Brother's Bride by Denise Hunter. Woodhaven Acres by Birdie L.
The Vicar's Daughter by Kimberley Comeaux. Bay Island by Beth Loughner. A Donut a Day by Gail Sattler.
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But For Grace by Tracey V. Banjo's New Song by Rosey Dow. Toni's Vow by Kay Cornelius. Redeemed Hearts by Cathy Marie Hake. The Tender Heart by Kristy Dykes. The Baby Quilt by Joyce Livingston. Loveswept by Tamela Hancock Murray. Ageless Love by Lauralee Bliss. Beguiling Masquerade by Carole Gift Page. Bayou Fever by Kathleen Y'Barbo. Temporary Husband by DiAnn Mills. Anita's Fortune by Kay Cornelius. The Birthday Wish by Joyce Livingston.
Ramshackle Rose by Cathy Marie Hake. Compassion's Charm by DiAnn Mills. A Single Rose by Pamela Griffin. Torey's Prayer by Tracey V. Changing Seasons by Colleen L. Eliza by Mildred Colvin. Out on a Limb by Gail Gaymer Martin. Double Deception by Lena Nelson Dooley. The Restoration by Cathy Marie Hake. Timing is Everything by Tracey V.
Dandelion Bride by Joyce Livingston. A Whale of a Marriage by Diann Hunt. Picture Imperfect by Nancy J. Mary's Choice by Kay Cornelius. Protecting Amy by Susan Page Davis. The Engagement by Kimberley Comeaux. Faithful Traitor by Jill Stengl. Michaela's Choice by Lisa Harris. Gerda's Lawman by Lena Nelson Dooley. Everlasting Hope by Tracey V. Basket of Secrets by Diann Hunt. Forever Friends by Tamela Hancock Murray.
Love's Image by Debby Mayne. Down from the Cross by Joyce Livingston. Silent Heart by Barbara Youree. Second Chance by Tracey V. This Child is Mine by Mildred Colvin. Hogtied by Lynn A. Renegade Husband by DiAnn Mills. Mother's Day by Joyce Livingston. Real Treasure by Tish Davis. Love's Denial by Tamela Hancock Murray. Taking a Chance by Kelly Eileen Hake. What's Cooking? Heartsong Presents by Gail Sattler. Escape to Sanctuary Heartsong Presents by M. Making Amends by Janet Lee Barton. The Hunt for Home by Ginny Aiken.
Remember Me by Kimberley Comeaux. Romanian Rhapsody by Darlene Franklin. Against the Tide by Rachel Druten. Alaskan Summer by Marilou H. Pirate's Prize by Lena Nelson Dooley. Love Worth Keeping by Joyce Livingston. Bayou Beginnings by Kathleen Miller. Hearts Twice Met by Freda Chrisman. Lambert's Code by Rachel Hauck. Journeys by Tamela Hancock Murray. Bah Humbug, Mrs. Scrooge by Joyce Livingston. Miss Menace by Nancy Lavo. Sooner or Later by Vickie McDonough.
Flash Flood by DiAnn Mills. Bayou Secrets by Kathleen Y'Barbo. Beside Still Waters by Tracey V. Lambert's Peace by Rachel Hauck. Rose Kelly by Janet Spaeth. Rebecca's Heart by Lisa Harris. Thunder Bay by Beth Loughner. Always a Bridesmaid by Andrea Boeshaar. Riches of the Heart by Tish Davis.
Bridal Veil by Cathy Marie Hake. With a Mother's Heart by Joyce Livingston. Bittersweet Remembrance by Gina Fields. Cry of My Heart by Linda Ford. Listening to Her Heart by Joyce Livingston. The Dwelling Place by Kathleen Miller. Mariah's Hope Heartsong Presents by M. A Gentle Fragrance by Pamela Griffin. Spoke of Love by Cathy Marie Hake. Anna's Journey by Nancy Toback. Merely Players by Kathleen E. Weaving a Future by Susan Page Davis. Christmas Mommy by Terry Fowler.
Adam's Bride by Lisa Harris. Wyoming Hoofbeats by Susan Page Davis. Lonely in Longtree by Jill Stengl. Safe in His Arms by Tish Davis. Deborah by Mildred Colvin. Golden Dawn by Cathy Marie Hake. Heart of the Matter by Kristy Dykes. Prescription for Love by Andrea Boeshaar. Golden Days by Mary Connealy. Three-dimensional TTE is a more reliable method for quantitative analysis, specifically for LV mass, volumes, and ejection fraction, and has superior reproducibility to two-dimensional TTE but much less prognostic validation. Abnormal LV geometry in hypertensive patients is frequently associated with diastolic dysfunction, , which can be further evaluated by a combination of transmitral flow and tissue Doppler studies.
Large artery stiffening is the most important pathophysiological determinant of isolated systolic hypertension and age-dependent increase in pulse pressure. A low ABI i. Hypertension is the second most important cause of CKD after diabetes. Hypertension may also be the presenting feature of asymptomatic primary renal disease. An alteration of renal function is most commonly detected by an increase in serum creatinine. This is an insensitive marker of renal impairment because a major reduction in renal function is needed before serum creatinine rises. The albumin:creatinine ratio ACR is measured from a spot urine sample preferably early morning urine , and is the preferred method to quantify urinary albumin excretion.
A progressive reduction in eGFR and increased albuminuria indicate progressive loss of renal function, and are both independent and additive predictors of increased CV risk and progression of renal disease. The prognostic significance of hypertensive retinopathy by fundoscopy has been well documented. Fundoscopy may be considered in other hypertensive patients. The increasing emergence of new techniques to visualize the fundus through smartphone technologies should increase the feasibility of more routine fundoscopy.
Hypertension increases the prevalence of brain damage, of which transient ischaemic attack TIA and stroke are the most dramatic acute clinical manifestations. In the asymptomatic phase, brain damage can be detected by magnetic resonance imaging MRI as white matter hyperintensities, silent microinfarcts, most of which are small and deep, i. Cognitive impairment in older patients is, at least in part, hypertension-related, and cognitive evaluation tests should be considered in the clinical assessment of hypertensive patients with a history suggestive of early cognitive impairment.
The Mini-Mental State Examination has been the most widely used method in clinical trials, but is now being superseded by more sophisticated cognitive tests that are more suitable for routine clinic visits. As discussed above, HMOD assessment may play a role in stratifying the risk of patients with hypertension.
In post hoc analyses, BP treatment-induced regression of some but not all manifestations of asymptomatic HMOD, as a consequence of treatment, is associated with a reduction in CV risk, thereby providing additional information on the effectiveness of treatment in individual patients. The information available on the sensitivity and timing of changes in HMOD during antihypertensive treatment is summarized in Table If, when, and how often the assessment of HMOD should be performed has not been validated in follow-up studies.
HMOD can also develop during the course of antihypertensive treatment, and this may be accompanied by increased risk. Sensitivity to detect treatment-induced changes, reproducibility and operator independence, time to changes, and prognostic value of changes provided by markers of hypertension-mediated organ damage.
Hypertension is a very common condition and most patients with hypertension, in most healthcare systems, will be managed in the primary care setting. However, there are circumstances in which a referral for routine hospital-based evaluation and treatment may be required, keeping in mind that in some instances out-of-office or office-based care of hypertensive patients depends on the healthcare organization of a given country: Patients in whom secondary hypertension is suspected see section 8.
Other clinical circumstances in which the referring doctor feels more specialist evaluation is required. There are also rarer circumstances in which a patient with hypertension should be referred to hospital for emergency care, which will often require inpatient care see section 8. Several genome-wide association studies and their meta-analyses have identified loci that are associated with BP regulation, but together these only explain about 3.
There are two well-established strategies to lower BP: lifestyle interventions and drug treatment. Device-based therapy is also emerging, but is not yet proven as an effective treatment option. Lifestyle interventions can undoubtedly lower BP and in some cases CV risk see section 7. The drug treatment of hypertension is founded on very solid evidence, underpinned by the largest number of outcome-based RCTs in clinical medicine. Relative outcome reductions calculated by two recent meta-analyses are similar to those provided by the original meta-analysis of the effects of BP lowering on outcomes in Another important objective of antihypertensive therapy is to reduce the development of CKD; however, the slow rate of decline in renal function in most hypertensive patients makes the demonstration of potential benefits of BP lowering difficult.
Consequently, the protective effect of BP reduction on kidney function can be less obvious and has been restricted to patients with diabetes or CKD, in whom there is a faster rate of disease progression. The recommendations that follow are based on outcome evidence from RCTs; however, it must be acknowledged that RCTs based on clinical outcomes have limitations, the most important of which are that the data are largely limited to older and high-risk patients, preferentially recruited to increase statistical power, and over a relatively short duration of follow-up, rarely beyond 5 years.
This means that recommendations for life-long treatment for younger and lower risk patients are necessarily based on considerable extrapolation. Big data, now being collected by national health system registries, health insurance companies, and prolonged observational follow-up of RCTs, are becoming an important source of long-term information on the effects of chronic treatment, which adds to that provided by observational studies over several decades.
All guidelines agree that patients with grade 2 or 3 hypertension should receive antihypertensive drug treatment alongside lifestyle interventions. New analyses and RCT data have become available in these important areas and are discussed below. Recent meta-analyses show significant treatment-induced reductions in CV events and mortality in patients with grade 1 hypertension. Furthermore, many of the patients had diabetes and were therefore at high CV risk. Based on these new data, this Task Force now recommends that lifestyle advice should be accompanied by BP-lowering drug treatment in patients with grade 1 hypertension at low—moderate CV risk.
Chronological age is often a poor surrogate for biological age, with consideration of frailty and independence influencing the likely tolerability of BP-lowering medications. Undoubtedly, there are RCTs showing outcome benefits with BP-lowering treatment in older patients whose baseline BP was in a lower SBP range, but these patients were often on background antihypertensive treatment, thus they cannot be defined as having true grade 1 hypertension. This is also the case for the data recently published from the SPRINT trial, which included a cohort of patients older than 75 years, in whom more intense BP lowering reduced the risk of major CV events and mortality.
It is well established that BP-lowering treatment withdrawal leads to a marked increase in CV risk. The previous Guidelines 17 recommended not to initiate antihypertensive treatment in people with high—normal BP and low—moderate CV risk.
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Therefore, these studies do not provide evidence to support treatment initiation in patients without hypertension. Another recent analysis, including patients with high—normal BP, concluded that primary preventive BP lowering was associated with reduced risk for death and incident CVD if baseline SBP was mmHg or higher, but at lower BP levels [i.
We recommend that patients with high—normal BP and low—moderate CV risk should be offered lifestyle advice, because this reduces their risk of progressing to established hypertension and may further reduce their CV risk. These patients should not be offered BP-lowering drug treatment. In these patients, monotherapy may be sufficient. Two recent meta-analyses of RCTs 8 , have shown that when BP-lowering data are stratified according to CV risk, the relative risk reductions do not differ across the various risk strata; not surprisingly, the absolute risk reduction is greater with increasing baseline CV risk.
These data have been taken as support for the hypothesis that BP-lowering treatment should be based on CV risk and target those at greatest CV risk, irrespective of their BP. The most effective strategy to reduce risk is to prevent the development of high CV-risk situations with earlier intervention. The assessment of CV risk is at the core of the treatment strategy recommended by these Guidelines because of the frequent coexistence of multiple CV risk factors in hypertensive patients, and to inform the use of concomitant medications e.
In patients with grade 2 or 3 hypertension, it is recommended that BP-lowering drug treatment should be initiated alongside lifestyle interventions. In patients with grade 1 hypertension at high risk or with HMOD, drug treatment should also be initiated simultaneously with lifestyle interventions. In lower-risk patients with grade 1 hypertension, BP-lowering drug treatment should be initiated after 3—6 months if BP is not controlled by lifestyle interventions alone Figure 3. Recommended BP thresholds for the initiation of antihypertensive drug treatment are shown in Table Treatment may be considered in these very high-risk patients with high—normal SBP i.
SBP — mmHg. In patients with grade 1 hypertension and at low—moderate-risk, drug treatment may be preceded by a prolonged period of lifestyle intervention to determine if this approach will normalize BP. The duration of the lifestyle intervention alone will depend on the level of BP within the grade 1 range, i. Initiation of blood pressure-lowering treatment lifestyle changes and medication at different initial office blood pressure levels.
Since then, new information has emerged from post hoc analyses of large outcome trials in patients at high CV risk, — registries in patients with coronary disease, and, more importantly, new RCTs and meta-analyses of all available RCT evidence. However, there were far fewer patients in these subgroups, and this last set of data will have been heavily influenced by the unusually low BP values in the SPRINT trial, due to the method of BP measurement see above. Importantly, this analysis showed consistent benefit from intensive BP lowering in patients at all levels of risk, including those with and without existing CVD, stroke, diabetes, and CKD.
Finally, in the first meta-analysis, the incremental benefit of BP lowering on events progressively decreased as the target BP was lowered. Furthermore, an additional meta-analysis by the same group found that permanent treatment discontinuation because of treatment-related adverse effects was significantly higher in those targeted to lower BP values.
Importantly, we specify a target range because the lower safety boundary assumes greater importance when BP is targeted to lower levels. RCTs in type 1 diabetes mellitus demonstrate that BP-lowering treatment has a renoprotective effect, but because these patients tend to be younger, previous RCTs have had inadequate power to study CV outcomes and to establish optimal BP targets.
In contrast, there have been many BP-lowering treatment RCTs, either exclusively dedicated to patients with type 2 diabetes or hypertension trials that have included a large cohort of patients with type 2 diabetes. However, the results have been less clear about whether a lower BP target is associated with further benefits. Although one recent meta-analysis concluded that most of the benefit associated with BP lowering was obtained at higher BP targets i. In summary, In patients with diabetes receiving BP-lowering drugs, it is recommended that office BP should be targeted to an SBP of mmHg, and lower if tolerated.
Attention should also be given to the consistency of BP control, because visit-to-visit BP variability is associated with increased CV and renal disease risk. Furthermore, CV protection has been found to be greater when BP control is accompanied by fewer visit-to-visit BP variations. The anticipated benefits vs. Although HYVET and most other RCTs in older patients have recruited relatively fit and independent patients, the SPRINT study also suggested that there are benefits of more intensive treatment being extended to older patients who are at the frailer end of the spectrum of patients meeting the recruitment criteria, with reduced gait speed.
Based on the new data, the targets suggested by the previous Guidelines now appear too conservative for many old and very old patients, especially those who are active and independent.
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Importantly, the impact of BP-lowering on the well-being of the patient should be closely monitored, because the increased risk of adverse events e. Further details on the approach to treatment of the frail older patient are discussed in section 8. This convergence has also been confirmed in treated patients in whom the difference between office BP and ambulatory BP values diminishes and becomes negligible at an SBP of approximately mmHg.
Heathy lifestyle choices can prevent or delay the onset of hypertension and can reduce CV risk. They can also augment the effects of BP-lowering therapy, but they should never delay the initiation of drug therapy in patients with HMOD or at a high level of CV risk. A major drawback of lifestyle modification is the poor persistence over time. The BP-lowering effect of sodium restriction is greater in black people, in older patients, and in patients with diabetes, metabolic syndrome, or CKD. The effect of reduced dietary sodium on CV events remains unclear.
However, they also reported that reducing sodium intake below a certain level about 3 g of sodium per day further reduced BP, but paradoxically was associated with an increased risk of all-cause and CV mortalities in both the general population and in hypertensive people, suggesting a J-curve phenomenon. There is no evidence from epidemiological studies that very low sodium intake may cause harm. Increased potassium intake is associated with BP reduction and may have a protective effect, thereby modifying the association between sodium intake, BP, and CVD.
Globally, usual sodium intake is between 3. We recommend sodium intake to be limited to approximately 2. Effective salt reduction is not easy and there is often poor appreciation of which foods contain high salt levels. Advice should be given to avoid added salt and high-salt foods. There is a long-established positive linear association between alcohol consumption, BP, the prevalence of hypertension, and CVD risk.
Binge drinking can have a strong pressor effect. Alcohol-free days during the week and avoidance of binge drinking 35 are also advised. Hypertensive patients should be advised to eat a healthy balanced diet containing vegetables, legumes, fresh fruits, low-fat dairy products, wholegrains, fish, and unsaturated fatty acids especially olive oil , and to have a low consumption of red meat and saturated fatty acids. A number of studies and meta-analyses — have shown that the Mediterranean diet is associated with a reduction in CV events and all-cause mortality.
With regard to coffee consumption, caffeine has been shown to have an acute pressor effect. Regular consumption of sugar-sweetened soft drinks has been associated with overweight, metabolic syndrome, type 2 diabetes, and higher CV risk. The consumption of these drinks should be discouraged. Excessive weight gain is associated with hypertension, and reducing weight towards an ideal body weight decreases BP. Weight reduction is recommended in overweight and obese hypertensive patients for control of metabolic risk factors, but weight stabilization may be a reasonable goal for many.
The Prospective Studies Collaboration concluded that mortality was lowest at a body mass index BMI of approximately Weight loss should employ a multidisciplinary approach that includes dietary advice, regular exercise, and motivational counselling. Weight loss can also be promoted by anti-obesity drugs and, to a greater degree, bariatric surgery, which appears to decrease CV risk in severely obese patients.
Epidemiological studies suggest that regular aerobic physical activity may be beneficial for both the prevention and treatment of hypertension, and to lower CV risk and mortality. A meta-analysis of RCTs, which rely on self-reported exercise and are by necessity unblinded, has shown that aerobic endurance training, dynamic resistance training, and isometric training reduce resting SBP and DBP by 3.
For additional benefit in healthy adults, a gradual increase in aerobic physical activity to min a week of moderate intensity or min a week of vigorous-intensity aerobic physical activity, or an equivalent combination thereof, is recommended. Smoking is a major risk factor for CVD and cancer.
Smoking is second only to BP in contributing risk to the global burden of disease, and smoking cessation is probably the single most effective lifestyle measure for the prevention of CVD, including stroke, myocardial infarction, and PAD. Most patients will require drug therapy in addition to lifestyle measures to achieve optimal BP control.
In the previous Guidelines, five major drug classes were recommended for the treatment of hypertension: ACE inhibitors, ARBs, beta-blockers, CCBs, and diuretics thiazides and thiazide-like diuretics such as chlortalidone and indapamide , based on: i proven ability to reduce BP; ii evidence from placebo-controlled studies that they reduce CV events; and iii evidence of broad equivalence on overall CV morbidity and mortality, with the conclusion that benefit from their use predominantly derives from BP lowering.
These conclusions have since been confirmed by recent meta-analyses. These Guidelines thus recommend that the same five major classes of drugs should form the basis of antihypertensive therapy. There are compelling or possible contraindications for each class of drug Table 20 and preferential use of some drugs for some conditions, as discussed below. There is also evidence that there are differences in the persistence and discontinuation rates of the major drug classes.
Other classes of drugs have been less widely studied in event-based RCTs or are known to be associated with a higher risk of adverse effects [e. These are useful additions to the antihypertensive armamentarium in patients whose BP cannot be controlled by proven combinations of the aforementioned major drug classes. They have similar effectiveness , as each other and other major drug classes on major CV events and mortality outcomes. This result halted further research into the clinical utility of aliskiren for BP treatment. ACE inhibitors are associated with a small increased risk of angioneurotic oedema, especially in people of black African origin and, in such patients, when RAS blockers are used, an ARB may be preferred.
CCBs are widely used for the treatment of hypertension and have similar effectiveness as other major drug classes on BP, major CV events, and mortality outcomes. Though clinically a very relevant event, it is a difficult endpoint to quantify precisely, either because symptoms and signs are relatively non-specific or because oedema due to CCBs may result in misdiagnosis. Comparison with diuretics may also be difficult because fluid loss may mask signs and symptoms of incipient heart failure rather than preventing it. CCBs have also been compared with other antihypertensive agents in HMOD-based trials, and are reported to be more effective than beta-blockers in slowing the progression of carotid atherosclerosis, and in reducing LVH and proteinuria.
CCBs are a heterogeneous class of agents. A smaller number of RCTs have compared non-dihydropyridines verapamil and diltiazem with other drugs, and meta-analyses evaluating the two subclasses vs. Diuretics have remained the cornerstone of antihypertensive treatment since their introduction in the s. Their effectiveness in preventing all types of CV morbidities and mortality has been confirmed in RCTs and meta-analyses.
Chlorthalidone and indapamide have been used in a number of RCTs showing CV benefits, and these agents are more potent per milligram than hydrochlorothiazide in lowering BP, with a longer duration of action compared with hydrochlorothiazide and no evidence of a greater incidence of side effects. Both thiazide and thiazide-like diuretics can reduce serum potassium and have a side effect profile that is less favourable than RAS blockers, which may account for their association with a higher rate of treatment discontinuation.
Potassium may attenuate these effects, and a recent study has shown that the adverse effect of thiazides on glucose metabolism may be reduced by the addition of a potassium-sparing diuretic. In such circumstances, loop diuretics such as furosemide or torasemide should replace thiazides and thiazide-like diuretics to achieve an antihypertensive effect. RCTs and meta-analyses demonstrate that when compared with placebo, beta-blockers significantly reduce the risk of stroke, heart failure, and major CV events in hypertensive patients.
They also exhibit a somewhat less favourable side effect profile than that of RAS blockers, with a higher rate of treatment discontinuation when assessed in real-life conditions. Finally, beta-blockers are not a homogeneous class. In recent years, the use of vasodilating beta-blockers—such as labetalol, nebivolol, celiprolol, and carvedilol—has increased.
Studies on nebivolol have shown that it has more favourable effects on central BP, aortic stiffness, endothelial dysfunction, etc. It has no adverse effect on the risk of new-onset diabetes and a more favourable side effect profile than classical beta-blockers, , including less adverse effects on sexual function. Bisoprolol, carvedilol, and nebivolol have been shown to improve outcomes in RCTs in heart failure; however, there are no RCTs reporting patient outcomes with these beta-blockers in hypertensive patients.
Centrally active drugs were widely used in the earliest decades of antihypertensive treatment when other treatments were not available, but are less frequently used now, principally because of their poorer tolerability relative to the newer major classes of drugs. Antihypertensive drugs, other than the major classes already discussed above, are no longer recommended for the routine treatment of hypertension, and are primarily reserved for add-on therapy in rare cases of drug-resistant hypertension where all other treatment options have failed.
Guidelines have generated a variety of different strategies to initiate and escalate BP-lowering medication to improve BP control rates. In previous Guidelines, the emphasis was on initial use of different monotherapies, increasing their dose, or substituting for another monotherapy. However, increasing the dose of monotherapy produces little additional BP lowering and may increase the risk of adverse effects, whilst switching from one monotherapy to another is frustrating, time consuming, and often ineffective. For these reasons, more recent Guidelines have increasingly focused on the stepped-care approach, initiating treatment with different monotherapies and then sequentially adding other drugs until BP control is achieved.
Despite this, BP control rates have remained poor worldwide. Several reasons need to be considered to identify why the current treatment strategy has failed to achieve better BP control rates: Efficacy of pharmacological therapies. Are the best available treatments, in whatever combination, incapable of controlling BP in most patients?
Physician or treatment inertia. Patient adherence to treatment. Evidence is accumulating that adherence is a much more important factor than previously recognised. Studies using urine or blood assays for the presence or absence of medication have shown that adherence to treatment is low. Insufficient use of combination treatment. BP is a multiregulated variable depending on many compensating pathways. Consequently, combinations of drugs, working through different mechanisms, are required to reduce BP in most people with hypertension.
Thus, monotherapy is likely to be inadequate therapy in most patients. Complexity of current treatment strategies. There is also evidence that adherence to treatment is adversely affected by the complexity of the prescribed treatment regimen. In a recent study, adherence to treatment was strongly influenced by the number of pills that a patient was prescribed for the treatment of hypertension.
The above considerations suggest that the most effective evidence-based treatment strategy to improve BP control is one that: i encourages the use of combination treatment in most patients, especially in the context of lower BP targets; ii enables the use of SPC therapy for most patients, to improve adherence to treatment; and iii follows a treatment algorithm that is simple, applies to all patients, and is pragmatic, with the use of SPC therapy as initial therapy for most patients, except those with BP in the high—normal range and in frail older patients see below.
Among the large number of RCTs of antihypertensive therapy, only a few have directly compared different two-drug combinations, with systematic use of the two combinations in both arms. In other trials, treatment was initiated using monotherapy in either arm and another drug and sometimes more than one drug was added, usually in a non-randomized fashion, according to a pre-specified treatment algorithm.
In a few trials, the design precluded the use of what might be considered optimal combinations because multiple monotherapies were being evaluated [e. With this caveat, Table 21 shows that a variety of drug combinations have been used in at least one active arm of placebo-controlled trials and have been associated with significant benefit on major CV events. In trials comparing different regimens Table 22 , all combinations have been used in a larger or smaller proportion of patients, without major differences in benefits.
The only exceptions are two trials in which a large proportion of the patients received either an ARB—diuretic combination or CCB—ACE inhibitor combination, with both regimens being superior to a beta-blocker—diuretic combination in reducing CV outcomes. However, in six other trials with seven comparisons , beta-blockers followed by diuretics or diuretics followed by beta-blockers were not associated with a significantly different risk of any CV outcome, , , , — and the beta-blocker diuretic combination was significantly more effective than placebo in three trials.
Major drug combinations used in trials of antihypertensive treatment in a stepped approach or as a randomized combination combinations vs. Based on the results of outcome RCTs and recent meta-analyses, and evidence of BP-lowering effectiveness, all five major drug classes can, in principle, be combined with one another, except for ACE inhibitors and ARBs, whose concomitant use may lead to no additional benefit but increased adverse effects and is thus discouraged. These combinations are now widely available in a single pill and in a range of doses, facilitating simplification of treatment, flexible prescribing, and uptitration from lower to higher doses.
These combinations will also limit potential adverse effects associated with diuretic or CCB monotherapy, reducing the risk of hypokalaemia due to diuretics and reducing the prevalence of peripheral oedema due to CCBs. These combinations also ensure that the RAS is inhibited as part of the treatment strategy, which is an important consideration for many patient groups e. Beta-blockers in combination should be preferentially used when there is a specific clinical indication for their use e. Initial combination therapy is invariably more effective at BP lowering than monotherapy, indeed even low-dose combination therapy is usually more effective than maximal dose monotherapy.
Although no RCT has compared major CV outcomes between initial combination therapy and monotherapy, observational evidence suggests that the time taken to achieve BP control is an important determinant of clinical outcomes, especially in higher risk patients, with a shorter time to control associated with lower risk. In this regard, the outcome of these real-life studies of the impact of initial combination therapy on adherence, BP control, and CV outcomes may be especially relevant.
A consideration in the current Guidelines was to persist with the current stepped-care approach to BP treatment, which has been interpreted as recommending monotherapy as initial therapy for most patients, reflecting current practice. In fact, the previous Guidelines did acknowledge the possibility of initial combination therapy for patients with grade 2 or 3 hypertension, or patients at high or very high risk. In other words, initial monotherapy was only recommended for grade 1 hypertension and low- or moderate-risk patients. Thus, in reality, the shift in emphasis in this new guidance is subtle.
However, normalizing the concept of initiating therapy with a two-drug combination for most patients with hypertension is likely to have a major effect on clinical practice and the speed and quality of BP control. Moreover, the possibility of starting with a low-dose combination of two antihypertensive drugs, even in grade 1 hypertensive patients with low—moderate-risk, is supported by the reduction of CV events obtained by combination therapy in the upper tertile grade 1 hypertension in the HOPE-3 trial.
Studies suggest that two-drug combination therapy will control BP in approximately two-thirds of patients. We do not recommend three-drug combinations as initial therapy. It is further supported by data from recent studies using various methods to assess adherence to treatment, including the quantification of antihypertensive drugs in urine and blood, , and estimates such as pill counting or prescription refills, which, although indirect, allow the measurement of adherence on a prolonged basis, thereby accounting for its time-variable nature.
This approach is now facilitated by the availability of several SPCs with a range of dosages, which eliminates the often-stated disadvantage of SPC therapy i. It is also convenient that the most widely available SPCs mirror the major drug class combinations recommended by these Guidelines. The major advantage of an SPC as the usual therapeutic approach for hypertension is that patients can progress from 1, 2, or 3 drug treatments whilst remaining on a simple treatment regimen with a single pill throughout, increasing the likelihood of adherence to therapy and achieving BP control.
Although, at present, the availability of two-drug SPCs is largely limited to a RAS blocker with either a CCB or diuretic, it would be desirable to see the development of an expanded range of low-cost SPCs in different drug formulations, tailored to different clinical requirements. Polypills have also emerged as SPCs i. Studies of bioequivalence suggest that when combined in the polypill, different agents maintain all or most of their expected effect.
Nevertheless, the advantage of treatment simplification and adherence suggests that use of the polypill may be considered in patients with hypertension as substitution therapy, when the need and effectiveness of each polypill component has been previously established by their administration in separate tablets. When BP remains uncontrolled with three-drug combination therapy, the patient is classified as having resistant hypertension, assuming that secondary causes of hypertension and poor adherence to treatment have been excluded, and that the elevation in BP has been confirmed by repeated office BP measurement, ABPM, or HBPM see section 8.
Such patients should be considered for specialist evaluation. Reflecting on the evidence above, and recognizing the urgent need to address the factors contributing to the poor control of BP in treated hypertensive patients see section 7. A beta-blocker in combination with a diuretic or any drug from the other major classes is an alternative when there is a specific indication for a beta-blocker, e.
The addition of spironolactone for the treatment of resistant hypertension, unless contraindicated see section 8. The use of other classes of antihypertensive drugs in the rare circumstances in which BP is not controlled by the above treatments. Information on availability and recommended doses of individual drugs, as well as SPCs and free combinations, can be found in national formularies.
The algorithm recommends initial therapy for most patients with a two drug-combination, ideally as an SPC. Variations from the core drug treatment algorithm for uncomplicated hypertension shown in Figure 4 are specified in Figures 5 to 8. Recommended BP target ranges for treated hypertension are shown in Table Refers to patients with previous stroke and does not refer to blood pressure targets immediately after acute stroke. Treatment decisions and blood pressure targets may need to be modified in older patients who are frail and independent.
Core drug treatment strategy for uncomplicated hypertension. Drug treatment strategy for hypertension and coronary artery disease. Drug treatment strategy for hypertension and chronic kidney disease. Drug treatment strategy for hypertension and hear failure with reduced ejection fraction. Do not use non-dihydropyridine CCBs e. Consider a loop diuretic as an alternative in patients with oedema. Drug treatment strategy for hypertension and atrial fibrillation. The drug treatment strategy for patients with hypertension should be based on the algorithm shown Figures 4 to 8 , unless there are contraindications to these drugs Table 20 , or concomitant conditions or diseases are present that require specific modification of the drugs, as outlined in the recommendations below.
Various device-based therapies have emerged, principally targeted at the treatment of resistant hypertension. These are discussed below. Carotid baroreceptor stimulation or baroreflex amplification therapy—externally via an implantable pulse generator or internally via an implantable device designed to increase the strain on the carotid bulb—can lower BP in patients with resistant hypertension. An RCT with the first generation of an implantable pulse generator showed sustained BP-lowering efficacy and sympathetic nervous system inhibition , but with some concerns about procedural and longer term safety.
A propensity score-matched comparison of the first- and second-generation systems revealed that BP at 12 months post-implantation was similar, with a better safety profile for the second-generation device. Another consideration is that implantation is costly and requires a complex surgical intervention. This has led to the development of an endovascular carotid baroreflex amplification device using a dedicated stent-like device designed to stretch the carotid bulb and increase baroreflex sensitivity.
Preliminary data in humans have shown evidence of BP-lowering efficacy of this new approach, but data from ongoing RCTs are needed to definitively understand its longer-term efficacy and safety. The rationale for renal denervation lay with the importance of sympathetic nervous system influences on renal vascular resistance, renin release, and sodium reabsorption, the increased sympathetic tone to the kidney and other organs in hypertensive patients, and the pressor effect of renal afferent fibres documented in experimental animals.
Several observational studies and national and international registries support the BP-lowering efficacy of renal denervation originally reported in the Symplicity HTN-1 and HTN-2 trials. The PRAGUE study documented similar effects between renal denervation and optimized pharmacotherapy mainly by adding spironolactone with respect to BP-lowering efficacy; however, the latter was associated with more side effects and high discontinuation rates. Beyond resistant hypertension, interim data in the first 80 patients treated with renal denervation but with no background antihypertensive therapy showed a modest effect of renal denervation vs.
Evaluating the efficacy of renal denervation has been challenging because the procedure needs to be applied to a population with a high probability of BP response. This is complicated by i the complex pathophysiology of hypertension, ii the lack of clinically applicable measures of sympathetic activity, iii the absence of predictors of the long-term BP response following renal denervation, and iv the absence of reliable markers of procedural success to immediately establish whether denervation has been achieved.
Except for rare problems related to the catheterization procedure access site complications, vessel dissection, etc. Major uncertainties remain as to the clinical role of renal denervation outside of clinical studies, which should be performed in carefully selected patients at specialist hypertension centres and by experienced operators. The central iliac arteriovenous anastomosis creates a fixed-calibre 4 mm conduit between the external iliac artery and vein using a stent-like nitinol device ROX arteriovenous coupler.
Some important safety aspects need to be considered. There were no reports of right heart failure or high-output cardiac failure after device implantation over the short-term, but longer follow-up is clearly needed. The carotid body is located at the bifurcation of the common carotid. It is innervated by nerve fibres from the vagus nerve through the cervical ganglion and the carotid sinus nerve. Surgical resection of the carotid body is associated with reductions in BP and sympathetic overactivity in patients with heart failure. In summary, device-based therapy for hypertension is a fast-moving field.
Further sham-controlled studies are needed before device-based therapies can be recommended for the routine treatment of hypertension outside of the framework of clinical trials. The recommended treatment strategy should include appropriate lifestyle measures and treatment with optimal or best-tolerated doses of three or more drugs, which should include a diuretic, typically an ACE inhibitor or an ARB, and a CCB.
Pseudo-resistant hypertension see below and secondary causes of hypertension should also have been excluded see section 8. After applying a strict definition see above and having excluded causes of pseudo-resistant hypertension see section 8. Poor office BP measurement technique , including the use of cuffs that are too small relative to the arm circumference, can result in a spurious elevation of BP. Marked brachial artery calcification , especially in older patients with heavily calcified arteries. Clinician inertia , resulting in inadequate doses or irrational combinations of BP-lowering drug therapies.
Other causes of resistant hypertension Lifestyle factors, such as obesity or large gains in weight, excessive alcohol consumption, and high sodium intake. Intake of vasopressor or sodium-retaining substances, drugs prescribed for conditions other than hypertension, some herbal remedies, or recreational drug use cocaine, anabolic steroids, etc. Resistant hypertension characteristics, secondary causes, and contributing factors adapted from reference A physical examination, with a particular focus on determining the presence of HMOD and signs of secondary hypertension.
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Laboratory tests to detect electrolyte abnormalities hypokalaemia , associated risk factors diabetes , organ damage advanced renal dysfunction , and secondary hypertension. Patients should be screened for a secondary cause of hypertension, especially primary aldosteronism or atherosclerotic renal artery stenosis, particularly in older patients or patients with CKD.
Poor adherence to treatment should be considered, but its identification may be challenging in routine clinical practice. Effective treatment combines lifestyle changes especially the reduction of sodium intake , discontinuation of interfering substances, and the sequential addition of antihypertensive drugs to the initial triple therapy. Ultimately, replacing all current drugs by a simpler treatment regimen using SPC treatment is recommended to reduce pill burden and improve adherence to treatment.
The optimal drug treatment of resistant hypertension has been poorly studied. The most effective strategy seems to be additional diuretic treatment to decrease volume overload, together with the restriction of salt intake, particularly in patients with CKD. BP control may be improved by increasing the dose of the existing diuretic or by switching to a more potent thiazide-like diuretic chlorthalidone or indapamide. Although resistant hypertension may show a BP reduction if the existing diuretic dose is further increased, most patients require the administration of additional drugs.
Moreover, the efficacy and safety of spironolactone for the treatment of resistant hypertension has not yet been established in patients with significant renal impairment. Moreover, electrolytes and eGFR should be monitored soon after initiation and at least annually thereafter. Neither was as effective as spironolactone, but they did reduce BP significantly vs.
Direct vasodilators, such as hydralazine or minoxidil, are infrequently used because they may cause severe fluid retention and tachycardia. New BP-lowering drugs nitric oxide donors, vasopressin antagonists, aldosterone synthase inhibitors, neutral endopeptidase inhibitors, and endothelin antagonists are all under investigation.
When spironolactone is not tolerated, replace with amiloride or eplerenone. Secondary hypertension is hypertension due to an identifiable cause, which may be treatable with an intervention specific to the cause. A high index of suspicion and early detection of secondary causes of hypertension are important because interventions may be curative, especially in younger patients [e.
Interventions that treat the cause of secondary hypertension later in life are less likely to be curative i. Screening all hypertensive patients for secondary hypertension is not feasible or cost-effective; however, there are some general patient characteristics that suggest those more likely to have secondary hypertension and in whom screening should be considered after confirming that BP is elevated with ABPM Table It is beyond the scope of these Guidelines to describe the detailed clinical management of specific causes of secondary hypertension.
However, the commoner causes of secondary hypertension, clinical history, and screening tests are described in Table 26 , and the typical age distribution of these causes of secondary hypertension is shown in Table Review of these tables demonstrates that most screening can be undertaken with blood and urine tests, abdominal ultrasound, and echocardiography. Referral to a specialist centre is recommended for additional investigations to confirm a suspected diagnosis of secondary hypertension and for clinical management.
Other causes of secondary hypertension due to drugs and substances, and rarer monogenic causes, are described below and are summarized in Tables 28 and Medications and other substances that may increase blood presssure Medications and other substances may cause a sufficient increase in BP to raise the suspicion of secondary hypertension Table Consequently, a careful drug history is important when considering a diagnosis of secondary hypertension.
Moreover, other commonly used drugs such as non-steroidal anti-inflammatory drugs or glucocorticoids can antagonize the BP-lowering effect of antihypertensive medications in patients treated for hypertension, and may contribute to a loss of BP control. Genetic causes of secondary hypertension are usually due to single-gene disorders see section 6. Thus, they are usually associated with a suppressed plasma renin concentration PRC or plasma renin activity PRA , which is unusual in younger patients and especially those treated with antihypertensive medications e.
Thus, the finding of a suppressed PRC or PRA, especially whilst taking these drugs, should raise the suspicion of secondary hypertension due a salt-retaining state. Importantly, beta-blockers in particular, but also non-steroidal anti-inflammatory drugs, alpha-methyl dopa, or clonidine, suppress PRC and PRA. Hypertension emergencies are situations in which severe hypertension grade 3 is associated with acute HMOD, which is often life-threatening and requires immediate but careful intervention to lower BP, usually with intravenous i. The hallmark of this condition is small artery fibrinoid necrosis in the kidney, retina, and brain.
Patients with severe hypertension associated with other clinical conditions who are likely to require an urgent reduction of BP, e. Patients with sudden severe hypertension due to phaeochromocytoma , associated with organ damage. The most common emergency symptoms will depend of the organs affected but may include headache, visual disturbances, chest pain, dyspnoea, dizziness, and other neurological deficits. In patients with hypertensive encephalopathy, the presence of somnolence, lethargy, tonic clonic seizures, and cortical blindness may precede a loss of consciousness; however, focal neurological lesions are rare and should raise the suspicion of stroke.
Acute stroke , especially intracerebral haemorrhage, when associated with severe hypertension has often been termed a hypertension emergency, but a more cautious approach is now recommended for acute BP lowering in the emergency setting of acute stroke see section 8. However, these patients will require urgent outpatient review to ensure that their BP is coming under control. Acute and severe increases in BP can sometimes be precipitated by ingestion of sympathomimetics such as meta-amphetamine or cocaine.
This can result in a hypertension emergency when there is evidence of acute HMOD. It is emphasized that many patients in an emergency department with acute pain or distress may experience an acute elevation in BP that will be restored to normal when the pain and distress are relieved, rather than requiring any specific intervention to lower BP. For patients with a suspected hypertension emergency, a diagnostic workup is shown in Table Apart from acute BP lowering in stroke, there are no RCTs evaluating different treatment strategies for hypertensive emergencies.
The key considerations in defining the treatment strategy are: Establishing the target organs that are affected, whether they require any specific interventions other than BP lowering, and whether there is a precipitating cause for the acute rise in BP that might affect the treatment plan e. The type of BP-lowering treatment required. With regard to drug treatment, in a hypertension emergency, i. Recommended drug treatments for specific hypertension emergencies , are shown in Table 31 and an expanded range of possible drug choices is shown in Table Rapid uncontrolled BP lowering is not recommended as this can lead to complications.
Hypertensive emergencies requiring immediate blood pressure lowering with intravenous drug therapy. Although i. However, low initial doses should be used because these patients can be very sensitive to these agents and treatment should take place in hospital. Further comprehensive details on the clinical management of hypertension emergencies are available.
The survival of patients with hypertension emergencies has improved dramatically over past decades, but these patients remain at high risk , and should be screened for secondary hypertension see section 8. After discharge from hospital, when BP has reached a safe and stable level on oral therapy, we recommend frequent, at least monthly, visits in a specialized setting until the optimal target BP is achieved and long-term specialist follow-up thereafter. As discussed in section 4, white-coat hypertension is defined as an elevated office BP despite a normal out-of-office BP.
Compared with normotensive people, white-coat hypertension is associated with an increased prevalence of dysmetabolic risk factors and asymptomatic organ damage. It is also associated with a greater risk of developing type 2 diabetes and sustained hypertension, as well as an overall increased risk of CV events. Office and out-of-office BP both home and ambulatory BP should be measured frequently, e. Treatment should consider lifestyle changes to reduce the elevated CV risk.
Whether or not patients with white-coat hypertension should receive antihypertensive drugs is unresolved. In white-coat hypertension, antihypertensive drugs have been shown to effectively and persistently lower office BP, with no concomitant reduction indeed, even a small increase of ambulatory BP values. However, it should be considered that people with white-coat hypertension have inevitably been well represented in trials documenting the protective effect of antihypertensive drugs, particularly those addressing conditions in which white-coat hypertension is more common, such as grade 1 hypertension or hypertension in older patients.
As reported in section 4. Such people usually have dysmetabolic risk factors and asymptomatic organ damage, which are substantially more frequent than in people who are truly normotensive. Masked hypertension is commoner in younger rather than older individuals, and in those with an office BP in the borderline hypertension range i. Masked hypertension is associated with progression to sustained office hypertension, increased frequency of developing type 2 diabetes, and the presence of HMOD. The long-term risk of fatal and non-fatal CV events approaches that of patients with sustained hypertension.
CV risk factors including organ damage and ideally both home and ambulatory BP should then be periodically monitored. Factors contributing to the out-of-office BP elevation e. The impact of antihypertensive drug treatment on CV outcomes in people with masked hypertension has never been studied. Nevertheless, treatment with BP-lowering medication should be considered because these patients are at high CV risk, often have HMOD, and the adverse prognostic importance of out-of-office BP elevations has been well documented.
Presently, no data are available from outcome trials for patients with MUCH; however, mindful of their high CV risk, treatment uptitration should be considered to ensure that that both office and out-of-office BP are controlled. The prevalence of hypertension increases with age.
Most hypertension across the age span is due to systolic hypertension; however, elevations of DBP and isolated diastolic hypertension, when they occur, are more common in younger rather than older patients. All younger adults with grade 2 or more severe hypertension should be offered lifestyle advice and drug treatment, as well as high-risk younger adults with grade 1 hypertension i.