Year Of Antihypertensive Therapy Research Articles

Risk of heart failure associated with thiazide diuretics compared with calcium channel blockers in patients with type 2 diabetes: a nationwide nested case-control study

Abstract Background Thiazide diuretics and calcium channel blockers (CCB's) are two important and widely used antihypertensive drugs classes among patients with type 2 diabetes (T2D). The risk of developing heart failure (HF) is increased in patients with T2D but whether use of these two drugs are associated with changes in HF risk is unknown. Purpose To examine and compare the association of two different classes of antihypertensive drugs, thiazide diuretics and CCB's, with the development of new onset HF in patients with T2D. Methods The study cohort comprised T2D patients >40 years on metformin and renin-angiotensin system inhibitor (RAS-i) without a history of HF or use of loop diuretics identified in Danish health care registers (period 1995 to 2015). A nested case-control study was conducted by matching all HF cases on sex, age and duration of T2D with 10 controls from the T2D population. Exposure was defined as three redeemed prescriptions of either a thiazide diuretic or a CCB up to 365 days before index, which corresponds to one year of antihypertensive therapy. Conditional logistic regression adjusted for comorbidities (atrial fibrillation, chronic obstructive pulmonary disease and anemia) was used to estimate and compare the treatment effect of thiazide diuretics and CCB's, with patients receiving neither of the two drugs as reference. Results The study population consisted of 170,514 T2D patients using metformin and RAS-i, comprising 13,814 HF cases each matched on sex, age and duration of T2D with 10 controls. The median age was 62 years and 55% were men. T2D patients, who had received antihypertensive treatment with only thiazide diuretics one year prior to index had a significantly lower risk of HF compared to the reference group who did not receive treatment with neither thiazide diuretics or CCB's: Hazard ratio (HR) 0.79 [95% confidence interval (CI) 0.74–0.85]. Patients who had received treatment with only CCB's had a comparable risk of HF: HR 0.98 [95% CI 0.94–1.02]. Patients who had received treatment with both thiazide diuretics and CCB's were not associated with a lower risk of HF: HR 1.01 [95% CI 0.96–1.08]. Conclusion Patients with T2D who received antihypertensive therapy with thiazide diuretics for at least one year had a significantly lower risk of HF compared to those who were not treated with either thiazide diuretics or CCB's. No association between use of CCB's and HF was observed. Use of thiazide diuretics may prevent development of HF in T2D and a randomized clinical trial evaluating diuretics is patients with T2D is warranted. Risk of new onset heart failure Funding Acknowledgement Type of funding source: None

Порівняння ефективності різних фіксованих комбінацій антигіпертензивних препаратів у хворих з артеріальною гіпертензією та гіпотиреозом

Мета роботи – оцінити ефективність різних фіксованих подвійних комбінацій антигіпертензивних препаратів та проаналізувати їх вплив на ремоделювання серця у хворих з артеріальною гіпертензією (АГ) та гіпотиреозом.Матеріали і методи. У дослідження увійшло 50 хворих з АГ та гіпотиреозом, яких розділили на дві групи методом сліпих конвертів по 25 осіб у кожній. Хворим 1-ї групи була призначена фіксована комбінація периндоприлу з індапамідом, хворим 2-ї групи – фіксована комбінація периндоприлу з амлодипіном. Групи статистично значуще не відрізнялися за віком хворих, тривалістю замісної гормональної терапії, тривалістю АГ, рівнем офісного систолічного і діастолічного артеріального тиску (АТ) при залученні в дослідження. За індексом маси тіла досліджувані групи були порівнянні, проте кількість пацієнтів з ожирінням була більшою у 2-й групі (p=0,05). Спостереження за хворими тривало 12 міс.Результати та обговорення. Отримані дані показали, що у хворих з АГ та гіпотиреозом досягнення еутиреоїдного стану сприяє зниженню рівня АТ, проте вимагає подальшого призначення антигіпертензивної терапії. Вивчені фіксовані комбінації антигіпертензивних препаратів, а саме периндоприлу з індапамідом та периндоприлу з амлодипіном, у хворих із АГ та супутнім гіпотиреозом забезпечують статистично значуще зниження АТ за результатами амбулаторного моніторування (р<0,05). При порівнянні ефективності комбінацій у хворих з АГ та гіпотиреозом залежно від індексу маси тіла встановлено, що комбінація периндоприлу з амлодипіном має більш виразний вплив на АТ у хворих з ожирінням.Висновки. Фіксована комбінація периндоприлу з амлодипіном порівняно з фіксованою комбінацією периндоприлу з індапамідом забезпечує статистично значуще більший вплив на регрес гіпертрофії міокарда лівого шлуночка, а саме зменшення індексу маси міокарда за зростом у степені 2,7 у хворих з ожирінням (р<0,01).

Изменение суточного ритма содержания ингибирующего лейкемию фактора в крови больных эссенциальной гипертензией

Leukemia inhibitory factor (LIF) exerts multidirectional effects in the setting of essential hypertension (EH). There is a mounting body of evidence refuting the postulate about identical STAT3 signaling in cardiomyocytes and endothelial/smooth muscle cells, which is important in the situation of extended exposure to gp 130 ligands (LIF in particular). At the same time, there are no reports on the circadian dynamics of peripheral blood LIF concentrations and possible secondary changes to the pathophysiological effects of this cytokine. This study aimed to analyze the circadian dynamics of LIF concentrations in the peripheral blood serum measured at 5 different time points in patients with stage II EH in the presence/absence of antihypertensive therapy and their relationship with the frequency of complications developing within a 5-year follow-up. Blood serum LIF was measured in 60 patients with stage II EH using ELISA at 8:00, 14:00, 20:00, 2:00, and 8:00 o’clock before putting the patients on antihypertensive therapy and one year after its onset. The identified patterns of diurnal LIF concentrations (a rise by ≥15% at 20:00, p < 0.001; a further rise by ≥22% peaking at 2:00, p < 0.001 relative to the values at 8:00) can be regarded as pathologic; their persistence after one year of antihypertensive therapy is a sign of EH progression and puts the patients at 6-fold risk for cardiovascular complications, including myocardial infarction and acute cerebrovascular events.

The change in the circadian rhythm of macrophage colony-stimulating factor content in the blood of patients with essential hypertension

The purpose of this research is to study the characteristics of the change in the circadian rhythm of macrophage colony-stimulating factor (M-CSF) content in the peripheral blood serum of patients with stage II essential hypertension (EH) based on 5 time points (8:00, 14:00, 20:00, 2:00, and 8:00) and analyze its connection with the frequency of cardiovascular events. Materials and methodsIdentified levels of M-CSF in the peripheral blood serum of 60 patients with stage II EH, before and after 1 year of antihypertensive therapy using enzyme-linked immunoassays (at 8:00, 14:00, 20:00, 2:00, and 8:00). ResultsThe research demonstrated that stage II EH patients with a medical case history lasting 10–14 years have a greater content of M-CSF in their peripheral blood serum (p > 0.001). Before the start of antihypertensive therapy, they also have an increased variability in the circadian rhythm of M-CSF content in the bloodstream (when compared with healthy individuals) due to an increase at 20:00, decrease at 2:00 and recovery at 8:00. In 70% of those patients taking antihypertensive medication and have reached their target arterial blood pressure, the cytokine decrease stabilizes at 2:00 but the increase at 20:00 remains unchanged. Thirty percent of patients retained the rhythm characteristics of M-CSF content in the blood serum typical of patients before the start of therapy. This is a predictor of an increase in the five-year risk of developing cardiovascular complications, particularly myocardial infarction and acute cerebrovascular accident, in individuals with a comparable risk of cardiovascular complications or death on the Framingham risk score.

Anemia is an independent risk factor for cardiovascular and renal events in hypertensive outpatients with well-controlled blood pressure: a subgroup analysis of the ATTEMPT-CVD randomized trial.

To investigate whether anemia is an independent risk factor for cardiovascular and renal events in hypertensive outpatients, we performed a subgroup analysis of the ATTEMPT-CVD study based on baseline hemoglobin. The ATTEMPT-CVD study was a multicenter, prospective, randomized study of hypertensive outpatients that compared the efficacy of angiotensin receptor blocker (ARB)-based antihypertensive treatment with non-ARB antihypertensive treatment over 3 years. In the present subanalysis, ATTEMPT-CVD study participants (n = 1213) were categorized into the anemic group and nonanemic group according to their baseline hemoglobin. We compared the anemic and nonanemic groups mainly in regard to the incidence of cardiovascular and renal events and blood pressure. We also performed a multivariable Cox proportional hazards analysis to determine the prognostic factors that were independently associated with cardiovascular and renal events. Of the 1213 patients enrolled in the ATTEMPT-CVD, 194 patients had anemia (mostly mild anemia) and 1019 patients did not. Blood pressure was well-controlled during the 3 years of antihypertensive therapy in both the anemic and nonanemic groups. However, the incidence of cardiovascular and renal events was significantly greater in the anemic group than in the nonanemic group (HR = 1.945: 95%CI 1.208-3.130; P = 0.0062). Even after adjustment, anemia was independently associated with cardiovascular and renal events (HR = 1.816: 95%CI 1.116-2.955; P = 0.0163) in overall hypertensive patients with well-controlled blood pressure. Anemia, even mild anemia, is an independent risk factor for cardiovascular and renal events in hypertensive outpatients whose blood pressure is well-controlled. Thus, anemia may be a novel therapeutic target for cardiovascular and renal diseases in hypertensive outpatients with anemia.

Neurocognitive Function in Children with Primary Hypertension after Initiation of Antihypertensive Therapy

To determine the change in neurocognitive test performance in children with primary hypertension after initiation of antihypertensive therapy. Subjects with hypertension and normotensive control subjects had neurocognitive testing at baseline and again after 1 year, during which time the subjects with hypertension received antihypertensive therapy. Subjects completed tests of general intelligence, attention, memory, executive function, and processing speed, and parents completed rating scales of executive function. Fifty-five subjects with hypertension and 66 normotensive control subjects underwent both baseline and 1-year assessments. Overall, the blood pressure (BP) of subjects with hypertension improved (24-hour systolic BP load: mean baseline vs 1 year, 58% vs 38%, P < .001). Primary multivariable analyses showed that the hypertension group improved in scores of subtests of the Rey Auditory Verbal Learning Test, Grooved Pegboard, and Delis-Kaplan Executive Function System Tower Test (P < .05). However, the control group also improved in the same measures with similar effects sizes. Secondary analyses by effectiveness of antihypertensive therapy showed that subjects with persistent ambulatory hypertension at 1 year (n = 17) did not improve in subtests of Rey Auditory Verbal Learning Test and had limited improvement in Grooved Pegboard. Overall, children with hypertension did not improve in neurocognitive test performance after 1 year of antihypertensive therapy, beyond that also seen in normotensive controls, suggesting improvements with age or practice effects because of repeated neurocognitive testing. However, the degree to which antihypertensive therapy improves BP may affect its impact upon neurocognitive function.

Assessment of Oxidative DNA Damage by Alkaline Comet Assay in Human Essential Hypertension.

The objective of the present study was to investigate the antioxidant status and the extent of oxidative DNA damage in lymphocytes and their relation with essential hypertension (EHT). A total of 100 South Indian subjects aged 30-65 were included for the study. Of these 50 were normotensive controls (group-1) with blood pressure ≥120/80mm Hg, 50 were newly diagnosed (group-2) and were not on any antihypertensive drugs, but had systolic blood pressure ranging between 140 and 160mmHg and diastolic blood pressure 95-100mmHg and 50 newly diagnosed essential hypertensive patients underwent drug therapy for 1year was considered as group-3. Enzymatic and non-enzymatic antioxidants significantly decreased and lymphocyte DNA damage was significantly increased in newly diagnosed hypertensive patients compared with control group. The major decrease in DNA damage and significant improvement in enzymatic and non-enzymatic antioxidants were observed after 1year of antihypertensive therapy in treated group compared with newly diagnosed hypertensive patients. Total antioxidant status and lymphocyte DNA damage showed a strong negative correlation in all the three groups. Essential hypertension associated with oxidative stress which in turn causes genotoxic susceptibility to variety of disease including cancer. In the absence of DNA repair process and DNA checkpoint mechanisms, the genomic integrity is susceptible to extensive damage. In our study, increased oxidative DNA damage and decreased antioxidant levels were frequently observed in the newly diagnosed essential hypertensive patients, suggesting that oxidative stress is important in the pathogenesis of EHT. Therefore, the present study has additional clinical implication. Further investigations with large number of patients along with antioxidant supplement are highly warranted.

Long-term use of angiotensin II receptor antagonists and calcium-channel antagonists in Algerian hypertensive patients: Effects on metabolic and oxidative parameters

The effects of calcium antagonists (amlodipine) and angiotensin II receptor antagonists (telmisartan) on lipid profile and oxidative markers were investigated in Algerian hypertensive patients. At the beginning and after 1 year of antihypertensive therapy, blood samples are collected for determination of biochemical parameters (glucose, cholesterol, triglycerides, urea, creatinine) and oxidative markers (malondialdehyde, carbonyl proteins, nitric oxide, superoxide anion, vitamin C, glutathione, catalase, superoxide dismutase). The results of this study indicate that telmisartan and amlodipine are effective antihypertensive agents in the treatment of hypertension because a significant reduction in systolic and diastolic blood pressure was observed in all hypertensive patients after 1 year of treatment. Our results show also that telmisartan and amlodipine treatments counteracted hypertension-dependent lipid abnormalities and oxidative stress. Telmisartan treatment appears to be more efficient than amlodipine treatment. In addition, telmisartan, which reversed all lipid and redox changes associated with hypertension, should be prescribed, especially in hypertensive patients with hypertriglyceridemia and with severe oxidative stress.

Estimated Glomerular Filtration Rate Reversal by Blood Pressure Lowering in Chronic Kidney Disease: Japan Multicenter Investigation for Cardiovascular DiseaseB CKD Study

Patients are diagnosed as having chronic kidney disease (CKD) if estimated glomerular filtration rate (eGFR) is <60 mL/min/1.73 m(2) . Low eGFR is likely to increase the incidence of cardiovascular events and lead to dialysis. Therefore, it is important to prevent eGFR from decreasing eGFR. However, it still remains unknown whether antihypertensive therapy can prevent low eGFR from becoming even lower and improve eGFR in hypertensive patients with CKD. The authors analyzed the results of the Japan Multicenter Investigation for Cardiovascular DiseaseB (JMIC-B) and investigated the effects of antihypertensive therapy on eGFR. In hypertensive patients with CKD (eGFR <60), eGFR was significantly increased from 51.87±6.21 (n=98) to 57.55±19.00 (P<.001) after 3 years of antihypertensive therapy. In patients without CKD (eGFR ≥60), eGFR was significantly decreased from 91.84±23.27 (n=682) to 88.95±23.67 (P<.001). Regardless of the type of antihypertensive drugs used, eGFR was significantly increased in patients with CKD and was significantly decreased in patients without CKD. This paper shows that antihypertensive therapy can improve eGFR in hypertensive patients with CKD. J Clin Hypertens (Greenwich). 2012;00:00-00. ©2012 Wiley Periodicals, Inc.

Oxidative stress in hypertensive children before and after 1 year of antihypertensive therapy

BackgroundThe relation between primary hypertension (PH), target organ damage (TOD) and oxidative stress (SOX) is not known.MethodsWe assessed SOX in 86 children with PH before and after 12 months of standard non-pharmacological and pharmacological therapy based on renin-angiotensin system blockade.ResultsPatients with left ventricular hypertrophy (LVH) and with carotid intima-media thickness (cIMT) >2SDS had higher thiobarbituric acid reactive substances (TBARS) concentrations in comparison to patients without LVH or with normal cIMT. Patients with metabolic syndrome (MS) had lower activity of gluthatione peroxidase, higher asymmetric dimethyloarginine (ADMA) and oxidized LDL cholesterol (oxyLDL) in comparison to patients without MS. TBARS correlated with left ventricular concentric hypertrophy, cIMT, albuminuria and SBP/24 h. ADMA and oxyLDL correlated with CRP and TG/HDL ratio. After 1 year of antihypertensive treatment blood pressure, TOD and prevalence of MS decreased. TBARS decreased and glutathione concentrations increased. The decrease of TBARS concentration correlated with the decrease of body mass index (BMI). Decrease of oxyLDL and ADMA correlated with increased insulin sensitivity, however markers of SOX did not correlate with BP decrease.ConclusionSOX in children with PH correlates with TOD, metabolic abnormalities, changes in fat amount and improvement of insulin sensitivity, but not with BP decrease.

Prevalence of residual left ventricular structural changes after one year of antihypertensive treatment in patients of African descent : role of 24-hour pulse pressure

One year of antihypertensive therapy may normalise left ventricular (LV) structure in 51% of hypertensive patients of European descent. Whether similar effects can be achieved in patients of African descent, who have a high prevalence of concentric LV hypertrophy (LVH) and remodelling, is unknown. In 103 hypertensive patients in the Baragwanath Hypertension study we evaluated the prevalence of residual LV structural changes (echocardiography) after four and 13 months of stepwise antihypertensive therapy. After 13 months of therapy, 24-hour blood pressure control was achieved in 47% of patients. At baseline, 51.5% of patients had concentric LVH, 19% eccentric LVH and 12% concentric LV remodelling. Despite changes in LV mass index (p < 0.01) and relative wall thickness (p < 0.05) with treatment, the proportion of patients with a normal LV mass or geometry increased only from 17.5 to 25% (p > 0.05), while 26% remained with concentric LVH (p < 0.001 compared to baseline), 25% with eccentric LVH and 23% with concentric LV remodelling (p < 0.05 compared to baseline). Residual structural changes were associated with 24-hour pulse pressure (p = 0.02), but not with 24-hour systolic or diastolic blood pressure or clinic blood pressure. Even after a year of antihypertensive therapy, a high proportion (74%) of hypertensives of African ancestry retained residual LV structural changes, an effect that was associated with 24-hour pulse pressure but not systolic or diastolic blood pressures or clinic blood pressure in this ethnic group.

Abstract 16804: Long-Term Differential Effects of Amlodipine and Atenolol based Antihypertensive Therapy on Left Ventricular Structure and Function: An ASCOT Sub-Study

Background: Both left ventricular hypertrophy (LVH) and impairment of LV diastolic function have been shown to be important predictors of morbidity and mortality in hypertension. Anti-hypertensive treatment can cause regression of LVH and improve LV diastolic function. However little is known about whether these changes are sustained with long term treatment. Methods: Six-hundred and sixty-nine patients (mean age 62 years, 78.9% male) in the ASCOT study who were randomised to either an amlodipine-based regimen (Amlod), or an atenolol-based antihypertensive regimen (Aten) had LV structure and diastolic function assessed by tissue Doppler echocardiography. Measurements were made a median time of 1.48 (Phase 1) and 3.49 (Phase 2) years after randomisation. Results: Blood pressure was lower in Amlod both at phase 1 (141/80 vs 146/83) and phase 2 (138/79 vs 143/82).Left ventricular mass index had significantly improved between Phase 1 and Phase 2 assessment in both treatment groups (Amlod: 119.6 to 116.6 g/m 2 , p=0.007, Aten: 121.8 to 117.2 g/m 2 , p&lt;0.001).At the initial Phase 1 assessment LV diastolic function was better in Amlod compared with Aten (e' 8.5cm/s versus 7.7cm/s, p&gt;0.001; E/e' 7.6 versus 8.1, p=0.008). With a further 2 years of antihypertensive therapy with good BP control there was a small, significant drop in e' but no change in E:e'with Amlod (e' Phase 2 8.1cm/s, versus phase 1 p&lt;0.001; E/e' Phase 2 7.8, versus phase 1 p=0.29); in contrast in Aten there was no change in e' but a small, significant rise in E:e' (e' Phase 2 7.7cm/s, versus phase 1 p=0.59; E/e' Phase 2 8.4, versus phase 1 p=0.02).By the end of the phase 2, after correction for age, gender and systolic blood pressure, e' in Amlod remained significantly higher than aten (p&lt;0.01). Conclusions: Patients with hypertension and good BP control had further regression of LV mass between 1.5 and 3.5 years of antihypertensive therapy with both Amlod and Aten. Those receiving Amlod had better echocardiographic indices of diastolic function at both time points when compared with Aten. Appropriate antihypertensive therapy may lead to early improvement of diastolic function and allow maintenance of a more normal pattern at longer follow-up with improvement in left ventricular mass. Character Count: 1926

Heart Failure Prevention Is the Best Option To Stem High Costs and Disease Burden

In this issue of Circulation: Cardiovascular Quality and Outcomes , Okin and colleagues1 report on the incidence of heart failure in a cohort of patients with hypertension enrolled in the Losartan Intervention for End Point Reduction in Hypertension (LIFE) study. This study, an international randomized trial, demonstrated that losartan, when compared with atenolol, provided superior reduction of events in high-risk patients with hypertension and no history of heart failure before enrollment.2 Over a 5-year follow-up period, the incidence of heart failure in blacks was 7%, significantly higher than the 3.1% incidence rate found in nonblack patients. This difference persisted even when appropriately adjusted for differences such as the heavier risk factor burden, younger age, sex, renal disease, diabetes mellitus, randomized treatment, incident myocardial infarction, in-treatment QRS duration, strain and left ventricular hypertrophy as measured by ECG, and diastolic and systolic pressure. Additionally, an echocardiographic substudy demonstrated adverse differences in left ventricular structure and performance after 2 years of antihypertensive therapy in blacks compared to nonblacks. Article see p 157 These findings are consistent with several previous reports detailing heart failure differences in blacks, who, when receiving their diagnosis of heart failure, are younger; have greater risk factor burden; are more overweight; and are more likely to have diabetes, renal disease, less coronary disease, and higher heart failure-related hospitalization and death rates than whites.3,4 Unique in this report is that the cohort is entirely high-risk patients with hypertension. The small numbers of black participants (497) compared with white participants (8199), and thus, small numbers of new heart failure cases in blacks, is an important recognized limitation. The definition of heart failure relied on predefined hospital-based criteria and confirmatory evidence of heart failure as a cause of death. Blacks more often have impaired medical access, and thus …

Low-dose spironolactone, added to long-term ACE inhibitor therapy, reduces blood pressure and urinary albumin excretion in obese patients with hypertensive target organ damage

For some hypertensive patients, conventional blockade of the renin-angiotensin-aldosterone system with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers does not adequately protect against target organ damage. This may be particularly true for hypertensive patients with obesity, a condition often associated with elevated aldosterone levels. We conducted a pre-post study of fixed, low-dose spironolactone (12.5 mg/d), added to chronic ACE inhibitor-based antihypertension regimens, in obese subjects with essential hypertension and preexistent target organ damage. Outcomes of interest were changes in blood pressure (office, 24-h, and nocturnal), urinary albumin excretion, and potassium. 21 subjects with mean age 57.3 +/- 7.1 years, BMI 32.4 +/- 3.4 kg/m2 and 12.0 +/- 7.0 years of antihypertensive therapy were enrolled. The mean aldosterone level before spironolactone treatment was 10.1 +/- 7.3 ng/dl, and over 40% of subjects had baseline levels greater than mean population levels. During 4 weeks of low-dose spironolactone, mean office (110.6 +/- 7.8 to 105.0 +/- 8.1 mmHg, p = 0.004), 24-hour ambulatory (100.6 +/- 9.4 to 95.5 +/- 7.1 mmHg, p = 0.03) and nocturnal (95.3 +/- 11.5 to 87.5 +/- 8.2, p = 0.004) blood pressures all declined significantly. Log urine albumin : creatinine ratios also significantly dropped during spironolactone treatment (p = 0.002); in multivariate analysis, this decline did not appear to be due to changes in blood pressure but was influenced by concomitant changes in estimated glomerular filtration rate. Both the reductions in blood pressure and albumin excretion reversed after withdrawal of spironolactone. Serum potassium levels were essentially unchanged by low-dose spironolactone (p = 0.9). A fixed, low-dose of spironolactone, added to chronic ACE inhibitor therapy, reduced blood pressure and urinary albumin excretion in obese subjects with hypertension and preexistent target organ damage. A relative hyperaldosteronism due to aldosterone escape and/or obesity may explain the beneficial effects of spironolactone therapy in this study.

Regression of echocardiographic left ventricular hypertrophy in relation to resolution versus persistence of electrocardiographic strain after one year of antihypertensive therapy: the LIFE study

Regression of echocardiographic left ventricular hypertrophy in relation to resolution versus persistence of electrocardiographic strain after one year of antihypertensive therapy: the LIFE study

The Multiple Isradipine/Diuretic Atherosclerosis Study: adverse events over 3 years of antihypertensive therapy with isradipine vs hydrochlorothiazide

The Multiple Isradipine/Diuretic Atherosclerosis Study: adverse events over 3 years of antihypertensive therapy with isradipine vs hydrochlorothiazide

Organization and efficacy of an out-patient hypertension clinic.

ABSTRACT. A description is given of the diagnostic and therapeutic routines at an out‐patient hypertension clinic. The efficiency of treatment in terms of BP control, patient adherence and frequency of side‐effects is presented. The patients were derived from a screening examination of a random third of an urban male population aged 47–54 years. Cut‐off points for hypertension were BP above 175 (systolic) or 115 (diastolic) mmHg on two separate occasions or current antihypertensive therapy. With these criteria, 11.2% of the population was considered hypertensive. Out of 686 hypertensive men, cared for at the clinic, only 4.2% defaulted during a two‐year follow‐up. At the second annual examination 83% had casual diastolic BP below 105 mmHg, with an average reduction of 10 mmHg. The antihypertensive therapy consisted of single drugs, a diuretic or a β‐adrenergic blocking agent, in 32% of the patients. Fifty per cent of the patients had a combination of two drugs; diuretics and β‐adrenergic blockers or β‐adrenergic blockers and hydralazine, while 14% had the triple combination of diuretics, β‐adrenergic blockers and hydralazine. Side‐effects so serious as to cause withdrawal of a drug occurred in 15% of the patients during the first year and in 3% during the second year of antihypertensive therapy.

Effects of blood pressure reduction on the structural vascular abnormality in skin and muscle vascular beds in human essential hypertension.

1. Vascular resistance at maximal vasodilatation was examined in two vascular beds in two groups of hypertensive patients and in normotensive control subjects before and during anti-hypertensive therapy in the hypertension groups. 2. In one group of twelve untreated patients with essential hypertension, examined with plethysmography and intra-arterial blood pressure recording, a significantly higher vascular resistance at maximal vasodilatation was found in the hands compared with normotensive control subjects matched for age, sex, weight and height. This indicated a structural vascular abnormality in the patient group. 3. After 5 years of anti-hypertensive therapy in the patient group the difference in vascular resistance between patients and control subjects had decreased significantly, indicating a reversibility of the structural vascular abnormality. 4. Vascular resistance at maximal vasodilatation was examined in the calves of twelve untreated patients with essential hypertension and fourteen normotensive control subjects. Plethysmographic technique and indirect blood pressure recordings were used. A significantly higher vascular resistance was found in patients than in control subjects, indicating a structural vascular abnormality also in this vascular bed. 5. Anti-hypertensive treatment for 6 months in the patient group did not change vascular resistance at maximal dilatation, indicating that the structural vascular abnormality remained. 6. During acute reduction of blood pressure in hypertension by means of trimethaphan infusion, blood pressure and blood flow to the hands were reduced proportionally with no change of vascular resistance at maximal vasodilatation. 7. This indicates that resistance at maximal dilatation was unaffected by the acute reduction of blood pressure, in contrast to the findings after prolonged reduction of blood pressure in this vascular bed.