Similarities and differences in the antihypertensive effect of two calcium antagonist drugs, verapamil and nifedipine.

The short- and long-term effects of two calcium channel blocking drugs, verapamil and nifedipine, on blood pressure, heart rate, plasma catecholamines, plasma renin activity, plasma volume and cardiac performance (echocardiography) were studied in essential hypertensive patients and in normal subjects. Verapamil, 160 mg orally, reduced blood pressure within 60 minutes in 22 hypertensive patients, but not in 12 normotensive subjects. Nifedipine, 10 mg sublingually, reduced blood pressure within 15 minutes in 19 hypertensive patients, but not in 7 normotensive subjects. Plasma noradrenaline was significantly increased both in normal subjects and in hypertensive patients only after nifedipine was administered. Verapamil (80 mg three times a day) first, and nifedipine (10 mg three times a day) thereafter, or vice versa, were given to 12 hospitalized hypertensive patients on a fixed sodium and potassium intake; the drugs produced similar blood pressure reductions, but heart rate and plasma catecholamines were increased only after nifedipine (p less than 0.05). Neither drug affected plasma volume, aldosterone or plasma renin activity. Long-term ambulatory treatment with verapamil (80 or 160 mg three times a day for 2 to 4 months) or nifedipine (10 mg three times a day for 2 months) produced changes in all variables that were similar to those observed in the hospital (controlled) study. Shortening fraction was significantly increased after nifedipine (p less than 0.05) but no change was observed after verapamil. In conclusion, blood pressure is effectively reduced by both verapamil and nifedipine; an appreciable adrenergic stimulation may be caused by nifedipine, but usually not by verapamil, and fluid retention, renin release or myocardial depression is not observed during verapamil or nifedipine treatment.

Relation between cardiac hypertrophy and forearm vascular structural changes before and during long-term antihypertensive treatment.

In patients with hypertension, structural changes develop in the heart and in the systemic arteries that have a significant role in the maintenance and gradual worsening of the hypertensive disease. Blood pressure, basal and post-ischemic "maximal" forearm blood flow (strain-gauge venous occlusive plethysmography), and echocardiographic left ventricular mass index were measured in 28 hypertensive patients (WHO class I or II, 23 men and five women, aged 26 to 59 years). Minimal vascular resistance (mean arterial pressure/peak blood flow) was taken as an index of vascular structural changes. The same measurements were made in a group of 14 patients before and after long-term antihypertensive treatment: in eight patients after six and 12 months of treatment with captopril (50 mg twice a day, plus 25 mg of hydrochlorothiazide per day if necessary) and in six patients after six months of treatment with nitrendipine (20 mg per day, plus 50 mg of atenolol per day if necessary). A significant but weak direct correlation was found between the degree of left ventricular hypertrophy and mean arterial pressure (r = 0.41) or minimal vascular resistance (r = 0.31). Thus, patients were categorized according to whether they had left ventricular hypertrophy or impaired blood flow; the results suggested that left ventricular hypertrophy may be detected earlier than increased minimal vascular resistance. After six months of treatment, both captopril and nitrendipine significantly reduced left ventricular mass index and minimal vascular resistance. Left ventricular mass index was normalized in 50 percent of the patients, whereas minimal vascular resistance was normalized in one patient only. After 12 months of treatment, left ventricular mass index was normalized in all patients; minimal vascular resistance was on the average further reduced but normalized in only one additional patient. Thus, regression of cardiovascular structure also seems to occur earlier in the heart.

Beneficial effects of one year's treatment with captopril on left ventricular anatomy and function in hypertensive patients with left ventricular hypertrophy.

This study evaluated by echocardiography (M-mode tracings, two-dimensional-guided) the effects of captopril administration for one year (25 to 50 mg twice a day, alone or in combination with hydrochlorothiazide when necessary) on left ventricular mass index, on systolic function at rest and during stress (hand grip for three minutes and cold pressor test for three minutes), and on diastolic function in 15 patients with essential hypertension (13 men and two women, aged 30 to 67 years) with left ventricular hypertrophy. In addition, supine and standing plasma catecholamine concentrations, plasma renin activity, and plasma aldosterone levels were measured. Examinations were performed during a placebo period and after three, six, and 12 months of captopril treatment. Blood pressure was significantly reduced (p less than 0.001), but heart rate did not change. Left ventricular hypertrophy was progressively reduced during treatment, mainly through reduction of left ventricular wall thickness. After one year, all patients had a normal left ventricular mass index (less than 120 g/m2). Before and during treatment, left ventricular systolic function, at rest and on maximal hand grip and cold pressor testing, evaluated on the basis of fractional shortening as related to end-systolic stress, was within the 95 percent confidence limits (calculated in a group of 25 normal subjects) in all 15 patients with essential hypertension. The percent increase in left ventricular dimensions during the diastolic rapid filling phase was significantly increased by treatment (p less than 0.05), indicating improvement of left ventricular relaxation. As expected, plasma renin activity was increased, plasma aldosterone levels were decreased, and plasma catecholamine concentrations did not change. These results indicate that long-term treatment with captopril has beneficial effects on left ventricular anatomy and function in patients with essential hypertension.

Adrenergic activity and left ventricular function during treatment of essential hypertension with calcium antagonists.

The effects of 2 calcium antagonist drugs, verapamil and nifedipine, on blood pressure, heart rate (HR), plasma catecholamines, plasma renin activity and some echocardiographic indexes of left ventricular anatomy and function were studied in 67 patients with essential hypertension. The short- and long-term antihypertensive effect of verapamil was not associated with significant changes in HR, plasma catecholamines or plasma renin activity; the decrease in blood pressure after nifedipine was associated with a significant increase in HR and plasma catecholamines (mainly noradrenaline) (p less than or equal to 0.05). These findings were confirmed in a crossover comparison in 12 hospitalized patients treated with verapamil and nifedipine for 8 days each. The dose of isoproterenol that increased HR by 25 beats/min was significantly increased during verapamil treatment (p less than 0.05) and decreased during nifedipine treatment (p less than 0.01). Stroke volume and shortening fraction increased slightly but significantly (p less than 0.05) with 3 months of nifedipine treatment, while no change was detected with verapamil treatment. Left ventricular mass was significantly decreased after effective antihypertensive treatment for 3 months with verapamil or nifedipine (p less than or equal to 0.05).

Angiotensin-converting enzyme inhibition, catecholamines and hemodynamics in essential hypertension.

Captopril was given to 15 unselected patients with essential hypertension (WHO II) at a dose range of 300 to 600 mg/day. Hemodynamic indexes (thermodilution) as well as levels of plasma norepinephrine, epinephrine, renin activity and aldosterone were determined simultaneously at the end of 2 weeks of placebo and after 8 weeks of captopril treatment. Systolic and diastolic arterial pressures were reduced significantly by treatment both supine (p less than 0.0025) and standing (p less than 0.0025). The diastolic arterial pressure was normalized (less than 95 mm Hg) in five patients and significantly reduced in four, whereas six patients were considered poor responders (mean arterial pressure decrease 10 mm Hg or less). The decrease in arterial pressure correlated significantly with the reduction in total peripheral resistance (r = 0.71), whereas cardiac index did not change and stroke index increased because of a slight decrease of heart rate. Plasma and urinary norepinephrine and epinephrine did not change during treatment. Moreover, the response of both heart rate and plasma catecholamines to upright posture was not altered by captopril treatment. Plasma renin activity increased and plasma aldosterone concentration decreased during treatment. These results suggest that inhibition of converting enzyme activity by captopril induces a reduction in arterial pressure through a reduction in total peripheral resistance. There was no evidence of an appreciable reduction in sympathetic nervous system activity during therapy.

Regression of structural alterations in hypertension.

Morbidity and mortality are higher in hypertensive patients who have already developed cardiovascular complications. Several prospective epidemiological and clinical studies have indicated that regression of cardiovascular alterations, preferably when still at an initial stage, is a desirable goal in the treatment of hypertension. Clinical assessment of cardiac hypertrophy may be precisely obtained with echocardiography. Structural vascular changes may be evaluated indirectly in man by measuring minimal vascular resistance from maximal blood flow and arterial pressure. The results of a large number of studies have indicated that in hypertensive patients a significant regression of cardiovascular structural changes may be obtained with several antihypertensive drugs, but they have not yet established whether a complete "normalization" may be really obtained. Further studies are needed to identify factors that modulate regression of cardiac and vascular smooth muscle hypertrophy. Most important, it still remains to be clarified whether regression of cardiovascular structural changes in hypertensives significantly improves prognosis per se independently from blood pressure reduction.

Extended release felodipine in essential hypertension. Variations in blood pressure during whole-day continuous ambulatory recording.

Intraarterial blood pressure (BP) monitoring during free ambulation (Oxford technique) was carried out in 12 essential mild-to-moderate hypertensive patients undergoing 4 weeks treatment with felodipine, 10 mg given once daily in an extended release formulation. Compared to placebo, felodipine significantly reduced systolic and diastolic blood pressure throughout 24 h. The greatest reduction was observed at 10 AM, 3 h after drug administration (-32 +/- 6/-24 +/- 5 mm Hg for systolic and diastolic BP, respectively, P less than .001). Hourly BP values remained significantly lower up to and including the 24th hour during felodipine extended release treatment (-18 +/- 5/-11 +/- 3 mm Hg, P less than .001). Felodipine extended release also reduced 24 h blood pressure variability, evaluated on the standard deviation of each hourly mean (from 16.3 +/- 0.9/12.6 +/- 0.6 to 13.4 +/- 0.6/10.4 +/- 0.6 mm Hg, P less than .01). Furthermore, absolute BP values dropped significantly at the peaks of dynamic exercise (bicycle ergometer: from 248 +/- 13/123 +/- 11 to 204 +/- 24/102 +/- 13 mm Hg, P less than .001), isometric exercise (hand grip: from 232 +/- 18/133 +/- 16 to 180 +/- 20/101 +/- 16 mm Hg, P less than .001), and cold pressor test (from 229 +/- 20/127 +/- 14 to 178 +/- 22/99 +/- 15 mm Hg, P less than .001). In conclusion, felodipine extended release exerts a good antihypertensive effect which is maintained for 24 h and reduces the level of blood pressure peaks reached under different physical stresses.

Renal and hemodynamic effects of atrial natriuretic peptide infusion are not mediated by peripheral dopaminergic mechanisms.

The possible involvement of peripheral dopaminergic mechanisms in the action of atrial natriuretic peptides was investigated in 10 subjects by administering 200 micrograms h-ANP 99-126 intravenously for 30 min during treatment with 50 mg carbidopa, a peripheral inhibitor of dopamine synthesis, every 8 h, or during placebo. Atrial natriuretic peptide (ANP) infusion during placebo was associated with a significant increase of diuresis, natriuresis, kaliuresis, urinary noradrenaline, and dopamine excretion. Plasma aldosterone significantly decreased. Blood pressure was slightly reduced. The administration of carbidopa significantly reduced urinary dopamine excretion but did not modify natriuresis, diuresis, indexes of adrenergic and renin-aldosterone system activity, blood pressure, or heart rate, both in basal conditions and in response to ANP infusion. We conclude that the effects of exogenous ANP administration are independent from dopaminergic mechanisms that involve the synthesis of dopamine outside the central nervous system, particularly in the kidney.

Reduction of left ventricular hypertrophy after longterm antihypertensive treatment with doxazosin.

The aim of this study was to evaluate the effect of antihypertensive treatment with doxazosin on left ventricular anatomy and function. Therefore, after 4 weeks of washout with placebo (phase 1), doxazosin (dosage range from 1 to 16 mg, plus hydrochlorothiazide when necessary) was given to 11 essential hypertensive patients (6 M, 5 F, age range 34-63 years) for 8 weeks (phase 2) in order to achieve diastolic blood pressure values less than 90 mmHg; this dosage was then maintained for a further 20 weeks up to the end of the study (phase 3). Blood pressure was significantly reduced (Anova P less than 0.05), while heart rate did not change. A significant reduction of left ventricular mass index (from 128.5 +/- 26 to 114 +/- 23 g/m2, at the end of phase 1 and 3 respectively, P less than .001)) was observed. Before and during treatment left ventricular systolic function, both at rest and during stress (handgrip and cold pressor tests), evaluated by fractional shortening as related to end-systolic stress, in every case within 95% confidence limits, was calculated in normal subjects. Diastolic function, as evaluated by the ratio between peak early and atrial velocities of transmitral flow examined by pulsed doppler was significantly improved. Plasma catecholamine concentrations, plasma renin activity and plasma aldosterone did not change. A significant reduction of plasma cholesterol concentration was observed. These results confirm that doxazosin is a well tolerated and effective antihypertensive drug, with a favourable effect on blood lipids and they indicate that its longterm administration can induce a significant reduction of left ventricular mass.

Angiotensin converting enzyme inhibition, parasympathetic activity and exercise in essential hypertension.

Reduced parasympathetic activity has been reported in essential hypertension. Converting enzyme inhibition seems to increase parasympathetic tone. In order to evaluate the effects of enalapril on parasympathetic control of heart rate, the authors studied ten mild-to-moderate essential hypertensive patients (7 F, 3 M), treated for 2 weeks with placebo and for 1 month with enalapril. Compared to placebo, enalapril significantly reduced blood pressure (p less than 0.005 at least, both systolic and diastolic), without any change in heart rate. Enalapril enhanced parasympathetic activity as judged by the increased variation of heart period (VHP) during regular breathing. VHP was derived during continuous ECG recording by the difference between the mean of all maximum and minimum R-R intervals, taken as a measure of respiratory sinus arrhythmia: the higher the VHP, the higher the parasympathetic cardiac influence and vice versa. The response to exercise, used as an index of sympathetic stimulation, was not modified by enalapril: the heart rate peak reached during either static (hand grip) or dynamic (bicycle ergometer) exercise and the slope of the increase in blood pressure were unchanged. Therefore, enalapril appears to increase parasympathetic tone in essential hypertension, without any interference with sympathetic adaptation to stress.

Effect of enalapril at rest and during isometric and dynamic exercise in essential hypertensive patients.

Vasodilator drugs reduce peripheral vascular resistance but lead to a secondary baroreflex-mediated chronotropic effect. After angiotensin-converting enzyme inhibition, blood pressure falls without associated tachycardia. In a previous study it was observed that enalapril increased vagal tone in essential hypertensive patients. In order to evaluate the effect of enalapril on sympathetic stimulation 10 mild to moderate hypertensive patients were studied during static (hand grip) and dynamic exercise (bicycle ergometer), after 2 weeks of placebo and after 1 month of treatment with 20-40 mg enalapril once daily. Enalapril significantly reduced blood pressure and the rate-pressure product at rest and at peak dynamic exercise. There was no effect on supine and maximal heart rate. Enalapril also significantly reduced blood pressure during hand grip, but did not interfere with the rate of the increase. Thus, enalapril does not seem to interfere with sympathetic adaptation to stress.

Efficacy of low-dose captopril given twice daily to patients with essential hypertension uncontrolled by a beta blocker plus thiazide diuretic.

Thirty-two patients with moderate to severe essential hypertension whose supine diastolic blood pressure (SDBP) was greater than or equal to 95 mm Hg following 2 weeks' treatment with the optimal dosage of beta blocker-diuretic combination were randomly assigned to the addition of either captopril 25 mg or 50 mg b.i.d. After 6 weeks' treatment, if patients were not normalized (SDBP less than 95 mm Hg), the dose of captopril was doubled for a further 6 weeks. The addition of captopril led to a significant fall in standing and supine diastolic and systolic blood pressure at the end of the sixth and twelfth week of treatment. There was no difference in the change in blood pressure between the two groups. At the end of the study SDBP was normalized in 66% of patients and a further 12.5% had their SDBP reduced by greater than 10%. Captopril 25 or 50 mg administered twice daily proved to be a very effective antihypertensive agent when added to a beta blocker-diuretic combination in patients resistant to optimal doses of these drugs.

Short term effect of captopril on microalbuminuria induced by exercise in normotensive diabetics.

OBJECTIVE: To investigate whether captopril has any effect on microalbuminuria induced by exercise in normotensive diabetic patients with early stage nephropathy. DESIGN: Randomised, double blind, crossover trial. SETTING: Outpatient department. PATIENTS: 22 diabetics with stage II nephropathy (urinary albumin excretion rate less than 20 micrograms/min; 15 with type I diabetes and seven with type II), 32 patients with stage III nephropathy (urinary albumin excretion rate 20-200 micrograms/min; 14 with type I diabetes and 18 with type II), and 10 normal subjects. INTERVENTIONS: Four exercise tests on a cycle ergometer: the first two under basal conditions and the third and fourth after subjects had received captopril (two 25 mg doses in 24 hours) or placebo (two tablets in 24 hours). END POINT: Exercised until 90% of maximum heart rate achieved. MEASUREMENTS AND MAIN RESULTS: Mean urinary excretion one hour after the first two exercise tests was 21 micrograms/min in normal subjects, 101 micrograms/min in diabetic patients with stage II nephropathy, and 333 micrograms/min in those with stage III nephropathy. Similar results were obtained after placebo. After captopril the urinary excretion rate one hour after exercise was significantly decreased in diabetics with stage II (36 micrograms/min) and stage III (107 micrograms/min) disease compared with placebo but not in normal subjects. Systolic and diastolic pressures were similar in the three groups after placebo and captopril had been given. CONCLUSIONS: Captopril significantly reduces microalbuminuria induced by exercise in normotensive diabetics without affecting systemic blood pressure. Captopril may reduce renal intracapillary pressure.

Etozolin monotherapy and combination with verapamil in essential hypertension.

A total of 1337 patients with mild to moderate essential hypertension were included in an open, multicentre trial to assess the response rate to the diuretic etozolin (200 mg once a day) and to verify whether the addition of the calcium antagonist verapamil (120 mg twice a day) in non-responders may have a favourable effect. Etozolin lowered diastolic blood pressure to below 95 mmHg in 67.8% of patients after 4 weeks of treatment and in 62.4% of patients after 12 weeks. The patients who failed to respond to etozolin were given verapamil (120 mg twice a day), and 72.8% of these patients showed a good response to the combined treatment. Normalization of blood pressure was achieved in 83.6% of the total patients. The incidence of side effects was 14.3%; withdrawal due to side effects was reported in 2.5% of patients. Abnormalities on the ECG were recorded in 5.5% of patients. No consistent metabolic or electrolyte change was observed. In conclusion, etozolin given at a dose of 200 mg once a day seems to be an effective and safe antihypertensive agent. Its antihypertensive effect remains unaltered for 12 weeks at least. The combination with verapamil may be effective in those who do not respond to etozolin alone.

Adrenergic activity and myocardial anatomy and function in essential hypertension.

In hypertension, changes of cardiac anatomy and function are not just a simple consequence of the increased pressure load. The sympathetic nervous system activity is one of the factors which may influence the cardiac performance, and possibly also the cardiac anatomy of hypertensive patients. Several clinical studies have provided evidence of a subset of patients, usually with mild or borderline hypertension, with an increased cardiac performance, higher plasma catecholamine concentrations and/or greater response to beta-adrenergic stimulation. Animal studies have strongly suggested a possible role of adrenergic factors in the development of left ventricular hypertrophy (LVH). In man, plasma catecholamines are usually higher in hypertensive patients with LVH, and a correlation between left ventricular mass and plasma noradrenaline has also been observed. An impaired response to beta-adrenergic stimulation has been reported in hypertensive animals and in patients with LVH. Several studies have also suggested that reversal of LVH may be more easily induced by those antihypertensive drugs that reduce, or at least do not stimulate, the sympathetic activity, although exceptions to this statement may be observed.

Continuous haemodynamic ambulatory monitoring in essential hypertension.

Haemodynamic ambulatory monitoring was derived from the intra-arterial blood pressure (BP) profile in 10 patients with essential hypertension. Stroke volume (SV) was computed beat by beat according to the following formula: X x PSA x (1 + St/Dt), where X is a correction factor, PSA is the area under the systolic portion of the pressure curve, St is the systolic and Dt the diastolic time. The X value was obtained in each patient by predetermining SV by thermodilution and solving the previous formula by X. The correlation between SV calculation and SV measured independently by thermodilution was highly significant: r values ranged from 0.85 to 0.92 (intercepts close to 0 and slopes close to 1) during different situations (supine, tilt, dynamic and static exercise). In five patients continuous haemodynamic ambulatory monitoring was obtained by applying the formula above to the intra-arterial tracing recorded with the Oxford technique. A computer program was developed in order to get BP, heart rate (HR), SV, cardiac output (CO) and total peripheral resistance (TPR) simultaneously. In these patients, the morning increase of BP was determined by an increase of both CO and TPR. Stroke volume increased slightly during the night, probably as a consequence of a reduced HR.

Long-term antihypertensive treatment may induce normalization of left ventricular mass before complete regression of vascular structural changes: consequences for cardiac function at rest and during stress.

In 14 essential hypertensive patients, aged 26-59 years, blood pressure, left ventricular mass index (LVMI), systolic function (M-mode echo, two-dimensionally guided), post-ischaemic 'maximal' forearm blood flow (strain gauge venous occlusion plethysmography), plasma renin activity, plasma catecholamines and aldosterone were measured before and after 6 and 12 months of treatment (eight patients were given captopril, 100 mg/day, + hydrochlorothiazide 25 mg/day in five patients, and six patients were given nitrendipine, 20 mg/day, + atenolol 50 mg/day in four patients). Minimal vascular resistance (mean blood pressure/peak forearm blood flow) was taken as an index of arterial structural changes. After 6 months of treatment significant reductions in blood pressure (P less than 0.001), LVMI (P less than 0.001) and minimal vascular resistance were observed. After 12 months of treatment blood pressure, LVMI and minimal vascular resistance were further reduced. The LVMI was normalized in nine cases and the minimal vascular resistance in two cases only. Aldosterone and plasma catecholamines did not change, whereas plasma renin activity was increased during captopril only. Before and during treatment the left-ventricular shortening fraction in relation to end-systolic stress in each patient at rest, and at peak of handgrip and cold pressor tests, fell within the 95% confidence limits of correlation obtained in normals. Thus, in essential hypertensives long-term treatment can induce normalization of LVMI before complete regression of arterial structural changes in the forearm. Left ventricular systolic function is preserved after normalization of LVMI, both at rest and during stress.

Left ventricular systolic function in relation to withdrawal of different pharmacological treatments in hypertensives with left ventricular hypertrophy.

We evaluated the left ventricular mass index (LVMI) and the functional response to cold pressor and handgrip tests in 74 untreated essential hypertensive patients and 26 age and sex-matched normals. The same measurements were repeated in 22 essential hypertensives after 6 and 12 months of treatment (captopril or nitrendipine, plus diuretic or beta-blocker in a few cases) and in 21 essential hypertensives after withdrawal of treatment, a reduction in the LVMI and a further increase in blood pressure. Left ventricular systolic function was evaluated by the relationship between left ventricular end-systolic stress and fractional shortening. Highly significant negative correlations, with similar slopes and intercepts, were found between end-systolic stress and fractional shortening under basal conditions, after regression of left ventricular hypertrophy and after withdrawal of treatment, both at rest and at the peak of stress tests. An examination of each point of the relation between end-systolic stress and fractional shortening showed that very few points were beyond the 95% prediction limits of the correlation obtained in normal volunteers. These results indicate that left ventricular systolic function is normal in most untreated essential hypertensives, and is usually well maintained after regression of left ventricular hypertrophy during long-term treatment as well as after withdrawal of treatment, both at rest and during an acutely induced afterload increase.

Dissociation of effects of hypertrophy from hypertension on cardiac beta-receptors in renovascular hypertensive rats.

Reduction in density of beta-adrenoceptors has been demonstrated in the hypertrophied left ventricle (LV) of renovascular hypertensive rats (RHR). In order to investigate the relative role of cardiac hypertrophy as distinct from hypertension, LV beta-receptors were determined in RHR four days after nephrectomy of the clipped kidney (RHR-Nx) when blood pressure was reduced but hypertrophy still evident; the results were compared with those obtained in age-matched untreated RHR and sham operated rats (SHAM). As expected, blood pressure (BP) was reduced four days after nephrectomy (150 +/- 3 versus 212 +/- 11 mmHg untreated RHR, P less than 0.001) but LV hypertrophy had not regressed (3.07 +/- 0.16 versus 3.58 +/- 0.24 mg/g, NS). Ventricular beta-receptor density was reduced in both RHR (1.601 +/- 0.078 pmol/g) and RHR-Nx (1.667 +/- 0.124 pmol/g) compared with SHAM (2.033 +/- 0.06 pmol/g, P less than 0.05 for both). The dissociation constant (Kd) was not different among the three groups. Thus, the reduction of beta-adrenergic receptors in the hypertrophied LV of RHR persisted even when BP was lowered by nephrectomy, suggesting that hypertrophy per se rather than hypertension accounted for that reduction in cardiac beta-receptors.

Interrelations of cardiac and arterial vascular wall hypertrophy in essential hypertension.

Structural vascular changes in the calf arteries and left ventricular mass were measured in 52 essential hypertensive patients (WHO I and II, 35 men and 17 women, age range 21-63 years). Left ventricular mass was measured on M-mode echocardiographic tracings. Structural vascular changes were evaluated indirectly by studying the minimal vascular resistance, calculated from mean arterial pressure and maximal (post-ischaemic) blood flow, measured by venous occlusion plethysmography. A statistically significant correlation between left ventricular mass and minimal vascular resistance was observed (r = 0.33, P < 0.05). The low correlation suggested that structural changes in the heart and in the systemic arteries did not develop simultaneously. In the subgroup of patients with minimal vascular resistance in the normal range, left ventricular hypertrophy was found in 15 out of 30 patients (50% of cases) whereas, in the subgroup of patients with high minimal vascular resistance, absence of left ventricular hypertrophy was found in six out of 22 patients (27% of cases). These results suggest that left ventricular hypertrophy more often precedes arterial structural changes in the calves.