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The passive stress-strain relationship of right ventricular papillary muscles from 10 normal and 9 experimental cats with short-term pressure-overload right ventricular hypertrophy-failure was examined by plotting the logarithm of instantaneous stress (ln sigma) against the natural strain calculated as ln(l/l0) where l = instantaneous length and l0 = length at zero force. Such a stress-strain relationship was well approximated by a linear relationship. The slope K obtained from this linear relationship was higher in the hypertrophy-failure muscles (normal, 15.01 +/- 0.87 (SEM); hypertrophy-failure, 31.79 +/- 4.09; P less than 0.005). The value of the intercept, ln C was similar in the two groups (normal, -4.33 +/- 0.20; hypertrophy-failure, -4.71 +/- 0.10). This analysis indicates the the ln sigma-natural strain relationship is linear in the papillary muscle and the slope of this relationship, an index of stiffness, is increased in hypertrophy-failure muscles. Using a three-element muscle model, it is shown that increased diastolic stiffness may contribute to the decreased systolic performance.
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PMID:Increased passive stiffness of short-term pressure-overload hypertrophied myocardium in cat. 16 Feb 6

Sixteen patients with initial diastolic blood pressure greater than or equal to 120 mm Hg were treated for 1 year with extended-release nifedipine [nifedipine-GITS (gastrointestinal therapeutic system)]. Serial changes in left ventricular mass index and associated alterations in left ventricular systolic function, left ventricular filling, plasma renin activity, atrial natriuretic peptide, and catecholamines were evaluated. Blood pressure was significantly reduced from 200 +/- 8/122 +/- 3 mm Hg (mean +/- SEM) to 144 +/- 5/89 +/- 2 mm Hg (p less than 0.0001) at 1 year. Eleven patients (69%) required only nifedipine-GITS for blood pressure control and 5 (31%) required the addition of chlorthalidone. After 6 months, the left ventricular mass index was significantly reduced by 19% from 121 +/- 8 to 96 +/- 7 g/m2 and this reduction was sustained at 1 year. Septal and posterior wall thicknesses were reduced from 13.4 +/- 0.1 to 11.2 +/- 0.04 mm and from 12.8 +/- 0.1 to 10.0 +/- 0.03 mm (p less than 0.001), respectively. Prevalence of left ventricular hypertrophy decreased from 63 to 25%. Left ventricular fractional shortening increased from 34 to 42% (p less than 0.05) and the relationship between fractional shortening and end-systolic stress did not change. Over the year of sustained blood pressure reduction, the peak velocity of early filling increased from 58 to 63 cm/s (p = 0.07), the peak velocity of late filling did not change, and the ratio of late to early peak velocity of left ventricular filling significantly decreased (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of nifedipine-GITS on left ventricular mass and left ventricular filling. 137 1

The effects of antihypertensive treatment with calcium antagonists or angiotensin-converting enzyme (ACE) inhibitors on the reversal of left ventricular hypertrophy and the left ventricular function in elderly hypertensive patients were examined. Twenty-four elderly hypertensive patients with cardiac hypertrophy, aged from 65 to 79 years (mean +/- SEM of 71 +/- 1 years), were treated with a calcium antagonist (nifedipine or nicardipine) or ACE inhibitor (captopril or enalapril) for 3 months. Thirteen patients had essential hypertension [EH: systolic blood pressure (SBP) greater than or equal to 160 mm Hg and diastolic blood pressure (DBP) greater than or equal to 90 mm Hg, aged 70 +/- 1 years] and 11 had isolated systolic hypertension (ISH:SBP greater than or equal to 160 mm Hg and DBP less than 90 mm Hg, aged 74 +/- 2 years). All patients underwent M-mode echocardiography to assess left ventricular mass index (LVMI) and left ventricular function (ejection fraction, EF) before and after 3 months of treatment. BP significantly decreased from 174 +/- 3/97 +/- 1 to 144 +/- 5/84 +/- 2 mm Hg in EH and from 167 +/- 3/82 +/- 2 to 144 +/- 4/74 +/- 2 mm Hg in ISH. The LVMI was also significantly reduced from 204 +/- 14 to 174 +/- 16 g/m2 in EH and from 179 +/- 14 to 156 +/- 12 g/m2 in ISH. EF showed no significant changes with treatment in either group. In elderly hypertensive patients, the antihypertensive treatment with calcium antagonist or ACE inhibitor reduced cardiac hypertrophy without any deterioration of left ventricular function in both essential hypertension and isolated systolic hypertension.
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PMID:Effects of antihypertensive treatment on cardiac hypertrophy and cardiac function in elderly hypertensive patients. 171 72

An analysis of heart rate (HR) variability (HRV) was based on quantifying the number and amplitude of HR fluctuations over long (8-30 cycles) and short (2-4 cycles) sequences of acceleration and deceleration-forming oscillations. The 'product' (number times amplitude) is an equivalent of the power spectrum in the frequency domain. In the time domain, positive correlations with HR were found for the number of long (L) sympathetic-mediated oscillations, whereas they were negative for short (S) vagally-mediated oscillations. The L/S ratio, an index of the autonomic nervous system (ANS) balance, closely paralleled the circadian HR values. HRV was studied in the ambulatory ECG of three groups of 15 normal adults (group I), 13 patients with left ventricular hypertrophy (LVH, group II) and 13 patients with heart failure (HF, group III). In basic conditions the mean HR was 77.1 +/- 1.9 beats min-1 (mean +/- SEM) in group I, 76.8 +/- 3.3 in II, 79.5 +/- 3.5 in III (P = NS). The different types of oscillations had smaller 24-h average values of the product in groups II and III than in group I, but the trends did not reach significance. However, the pooled 24 hourly values of the L/S ratio in group I (1.17 +/- 0.09) were lower than in group II (1.33 +/- 0.06, P less than 0.05 at Ancova) and higher than in group III (1.06 +/- 0.09, P less than 0.001). A 3-day treatment with acebutolol non-uniformly slowed the mean HR:--9.5% in group I, --18.1% in II and -19.1% in III (P less than 0.001), and uniformly diminished the L/S ratio by 17% to 20% (P less than 0.01). In conclusion, the sympathetic predominance of the ANS balance in LVH and HF is reflected by the beta-blockade induced HR decrease that is twice as marked in patients as in controls. In basic conditions HRV tends to be depressed in LVH and even more in HF. The ANS imbalance, however, has different modalities depending on the presence of HF, probably because of the different status of beta-adrenergic receptors in this condition.
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PMID:Heart rate variability in left ventricular hypertrophy and heart failure, and the effects of beta-blockade. A non-spectral analysis of heart rate variability in the frequency domain and in the time domain. 182 32

Adaptations to left ventricular (LV) structure and function appear to be dependent on the type, intensity and duration of exercise training. We therefore studied two clearly defined groups of elite athletes, by M-mode and Doppler echocardiography, with a group of inactive individuals as controls. All groups were age matched. Group 1 comprised ten elite endurance athletes with maximal oxygen consumption (VO2 max) of 74.7 +/- 1.43 (mean +/- SEM). Group 2 consisted of ten elite weightlifters with VO2 max 45.3 +/- 2.00. Group 3 comprised of ten inactive individuals with VO2 max 44.5 +/- 2.13. Left ventricular end diastolic dimension was significantly higher in group 1 (5.72 +/- 0.07) than in groups 2 or 3 (5.29 +/- 0.09 and 5.19 +/- 0.09 respectively, p less than 0.001). Left ventricular mass index was significantly higher in groups 1 and 2 (156.4 +/- 5.97 and 138.6 +/- 7.27 respectively) than in group 3 (104.1 +/- 3.16 p less than 0.001). Percentage fractional shortening was used as an index of systolic function and no significant difference was found between groups. Doppler E:A ratio was taken as an index of diastolic function and was found to be significantly elevated in group 1 at rest (3.37 +/- 0.24) compared with 2.38 +/- 0.16 and 1.99 +/- 0.10 in groups 2 and 3 respectively (p less than 0.003). On exercise, the E:A ratio in group 1 was significantly higher than in group 3 (1.95 +/- 0.14 and 1.23 +/- 0.05 respectively p less than 0.001), and tended to be higher than group 2 (1.68 +/- 0.15 p = ns). These data show that both modes of intense training produce left ventricular hypertrophy. Diastolic function is not impaired in the athletes and may be augmented in the endurance athletes.
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PMID:A comparative study of left ventricular structure and function in elite athletes. 183 26

To study the cardiac determinants of regression of left ventricular hypertrophy in hypertension, left ventricular mass, fractional shortening and end-systolic wall stress were measured echocardiographically in 36 patients with essential hypertension and left ventricular hypertrophy. The patients were classified into two groups. Group I consisted of 15 patients with subnormal end-systolic wall stress, and Group II consisted of 21 patients with normal end-systolic wall stress. There were no significant differences between groups in systolic or diastolic blood pressure. After treatment for 4.4 +/- 1.7 years, echocardiographic studies were repeated. There were no significant differences between groups in the duration of the follow-up period and the kinds of antihypertensive drugs. After treatment, blood pressure decreased significantly in both groups (p less than 0.001 for both), with no significant difference between groups. Left ventricular mass increased significantly in Group I (from 331 +/- 7 to 363 +/- 24 g, mean +/- SEM, p less than 0.05), whereas it decreased significantly in Group II (from 318 +/- 16 to 268 +/- 17 g, p less than 0.001). Myocardial contractility (the relation between end-systolic wall stress and fractional shortening) remained almost the same as before treatment. In conclusion, in patients with hypertensive ventricular hypertrophy with subnormal end-systolic wall stress (inappropriate hypertrophy, probably induced by a neurohumoral factor), a decrease in blood pressure with antihypertensive treatment does not lead to regression of left ventricular hypertrophy, but rather to an increase in left ventricular mass.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac determinants of regression of left ventricular hypertrophy in essential hypertension with antihypertensive treatment. 213 79

Long-term survival of blacks with angiographically defined coronary artery disease was examined in a series of 1233 consecutive patients who underwent cardiac catheterization at a large urban municipal hospital. Vital status information was available at a mean of 86 weeks for the cohort as a whole, and 94 deaths were recorded. As noted in other angiographic series that included blacks, a high proportion of patients in this study had unobstructed coronary arteries (41%), and there was a preponderance of women (56%). Hypertension was present in 82% of the cases, whereas 68% of the sample had left ventricular hypertrophy as revealed by echocardiogram. The cumulative proportion of patients who were surviving at 5 years was 90 +/- 1 (+/- SEM), 79 +/- 4, and 70 +/- 4 for patients with no obstructive lesions, one-vessel disease, and multivessel disease, respectively. The survival rate at 3 years for patients who had undergone bypass surgery (N = 152) was only 82% (+/- 5%). Noninvasive univariate predictors of mortality included male sex, history of myocardial infarction, Q waves on electrocardiogram, exercise duration on treadmill stress testing, and left ventricular hypertrophy. Angiographic predictors included left ventricular end-diastolic pressure, the number of diseased coronary vessels, ejection fraction, and mean pulmonary artery pressure. Regression analysis showed an independent association for all the angiographic variables noted previously as well as for echocardiographically determined left ventricular hypertrophy. Survival rates for blacks with coronary artery disease in this series were considerably lower than those currently reported for whites, particularly for patients who underwent coronary bypass grafting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Survival determinants in black patients with angiographically defined coronary artery disease. 213 59

1. Blood pressure, left ventricular mass and platelet cytosolic free calcium concentrations were measured in 23 patients with untreated primary hyperparathyroidism, 30 normotensive control subjects and 23 control subjects matched for age, sex and blood pressure. In 12 patients measurements were repeated after parathyroidectomy. 2. Patients with primary hyperparathyroidism had significantly elevated blood pressures (139 +/- 6/86 +/- 3 mmHg, mean +/- SEM) compared with control subjects (125 +/- 2/78 +/- 1 mmHg), but high values persisted after hypercalcaemia was corrected. 3. Despite chronic extracellular hypercalcaemia, intracellular free calcium levels were lower in patients with hyperparathyroidism than in controls matched for age, sex and blood pressure (median concentrations 81.5 nmol/l vs 93 nmol/l, 95% confidence interval 0.1 to 20.1; P less than 0.05) and values tended to increase after parathyroidectomy. 4. Left ventricular mass index was increased in the primary hyperparathyroid group as compared with control subjects matched for age, sex and blood pressure (123 g/m2 vs 100 g/m2, 95% confidence interval -36.1 to -3.1; P = 0.03). Parathyroidectomy resulted in a small reduction of the left ventricular mass index (123.5 g/m2 vs 104 g/m2, 95% confidence interval 46.5 to 2.5; P = 0.1) but no change in blood pressure. 5. Hypertension and left ventricular hypertrophy in primary hyperparathyroidism are associated with relatively low levels of free calcium in platelets.
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PMID:Blood pressure, left ventricular mass and intracellular calcium in primary hyperparathyroidism. 215 37

1. To investigate the mechanisms leading to enhanced synthesis and release of atrial natriuretic factor during chronic hypoxia, we measured immunoreactive plasma atrial natriuretic factor, blood gases, packed cell volume, pulmonary artery pressure and systemic artery pressure in male Sprague-Dawley rats exposed to 1, 2 or 3 weeks of normobaric hypoxia. Rats were implanted with pulmonary and carotid artery catheters and studied conscious, 23 h after return to hypoxia. 2. The concentration of atrial natriuretic factor messenger RNA was measured in the right and left ventricular free walls of rats exposed to 3 weeks of hypoxia and in normoxic control rats. 3. There was a trend for plasma atrial natriuretic factor to increase with the duration of exposure to hypoxia but only the 3-week hypoxic rats had a significantly higher level (1080 +/- 193 pg/ml) than the normoxic control rats (318 +/- 46 pg/ml, P less than 0.05, mean +/- SEM). When all the data from normoxic and hypoxic rats were considered together, plasma atrial natriuretic factor was positively correlated with packed cell volume (r = 0.66, P less than 0.001), pulmonary artery pressure (r = 0.68, P less than 0.002), and the index of right ventricular hypertrophy (r = 0.54, P less than 0.01), but after analysis of partial correlation, packed cell volume was the only independent contributing factor to the variance in the level of plasma atrial natriuretic factor (r2 = 0.24).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Synthesis and secretion of atrial natriuretic factor during chronic hypoxia: a study in the conscious instrumented rat. 216 93

STUDY OBJECTIVE - The aim of the study was to examine the effects of antihypertensive drugs on heart and resistance vessels to see whether regression of peripheral vascular hypertrophy accompanies reduction in cardiac mass. DESIGN - Matched groups of spontaneously hypertensive and control rats were treated for 12 weeks with captopril (average dose 65 mg.kg-1.d-1) or hydrochlorothiazide (73 mg.kg-1.d-1) and compared to untreated groups. Perfusion pressure, which has been validated as an index of hypertrophy of resistance vessels, was determined in hind limbs of pithed rats at constant blood flow and maximum vasodilatation. SUBJECTS - Experimental animals were 14 week old male spontaneously hypertensive (SHR) rats (n = 41) and strictly age matched Wistar Kyoto rats (n = 12). SHR rats were assigned at random to three groups: (a) captopril treated (n = 15), (b) hydrochlorothiazide treated (n = 15), (c) control (n = 11). MEASUREMENTS and RESULTS - Mean perfusion pressure was 29.5(SEM 0.4) mm Hg in untreated Wistar Kyoto rats and 37.4(0.5) mm Hg in untreated SHR rats. In comparison with untreated SHR rats, treatment with captopril lowered blood pressure, perfusion pressure [35.2(0.3) v 37.4(0.5) mm Hg, p less than 0.01)], and left ventricular to body weight ratio [2.28(0.03) v 2.63(0.05) mg.g-1, p less than 0.01)]. Treatment with hydrochlorothiazide also lowered blood pressure but had no significant effect on left ventricular weight to body weight ratio [2.54(0.04)]. However, perfusion pressure was reduced to 35.3(0.5) mm Hg, p less than 0.01. CONCLUSIONS - For equal regression of vascular hypertrophy, captopril and hydrochlorothiazide had different effects on regression of left ventricular hypertrophy. Thus left ventricular and vascular structural changes may respond differently to the same drug in the same animal.
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PMID:Effects of antihypertensive drugs on heart and resistance vessels. 218 38


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