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We characterized the influence of the size of the left ventricular (LV) chamber (LV diastolic diameter, LVDD) and LV end-diastolic pressure (LVEDP) on left atrial active stroke index (LAASI) in patients with old myocardial infarction (OMI) (n = 118) and controls (n = 25). Patients with OMI were classified into four groups according to the grade of LVDD (> or = 55 or < 55 mm) and LVEDP (> or = 18 or < 18 mmHg). LAASI was determined by multiplying the LV stroke index by the fraction of left atrial active contraction of the velocity-time integral on the pulsed-wave Doppler echocardiogram. LAASI in the "LVDD > or = 55 & LVEDP > or = 18" group was less than that in the groups with normal LVEDP. LAASI did not differ among the normal LV dimension groups. The combination of LV enlargement and high LVEDP was related to the decrease in LAASI in patients with OMI.

The distensibility of the forearm veins in 24 patients with congestive heart failure was studied by occlusion plethysmography. Relationships between forearm venous distensibility and symptoms, hemodynamic data obtained by right heart catheterization and plasma levels of vasoactive hormones were evaluated. Forearm venous pressure (VP) and volume change (delta V) were measured simultaneously by the venous occlusion technique with strain gauge plethysmography. The relationship between venous pressure and volume change was fitted by the equation VP = c* exp (k* delta V) (r = 0.98 +/- 0.01) and the venous stiffness constant (k) was calculated. Venous volume change at a venous pressure of 20 mmHg (V20) was also measured as another index of venous compliance. The pressure-volume curve of the peripheral veins shifted leftward on the volume axis and the stiffness constant (k) increased as the New York Heart Association functional class grade increased. Mean pulmonary arterial pressure and pulmonary vascular resistance were closely related to k (r = 0.74, p less than 0.001; r = 0.73, p less than 0.001, respectively), and less closely to V20 (r = -0.56, p less than 0.004; r = -0.59, p less than 0.002, respectively). K and V20 were also related to stroke index (r = -0.57, p less than 0.004; r = 0.44, p less than 0.03, respectively) and stroke work index (r = -0.47, p less than 0.02; r = 0.45, p less than 0.03, respectively). K was also related to heart rate (r = 0.55, p less than 0.007), pulmonary capillary wedge pressure (r = 0.54, p less than 0.02), right atrial pressure (r = 0.51, p less than 0.02), cardiac index (r = -0.45, p less than 0.03), and systemic vascular resistance (r = 0.45, p less than 0.03). Both indexes were related to the plasma level of norepinephrine (r = 0.64, p less than 0.008; r = -0.52, p less than 0.04, respectively). We concluded that the venous tone was related to the severity of heart failure, especially to the symptoms, pulmonary arterial pressure and plasma concentration of norepinephrine, and that the venous stiffness constant, k, was a better parameter with which to assess peripheral venous tone.

Both myocardial contractility and contraction duration were assessed load-independently in isolated hypertrophic and control rat hearts. Hemodynamic parameters for isolated isovolumically contracting hearts were compared for 7 Wistar rats with DOCA-salt induced hypertrophy (LVH) and 7 controls. Loads were altered by changing the volume of an intraventricular balloon. Myocardial contractility was assessed in terms of the shortening-afterload (Sm-sigma aft), and the ejection fraction-afterload (EF-sigma aft) relations at common preloads, based upon the systolic myocardial stiffness concept. Indices of contraction duration (time to maximum stiffness, pressure time integral divided by peak pressure and the time required for left ventricular (LV) peak pressure to be reduced by a half) were prolonged in LVH. Multiple regression analyses indicated that the degree of hypertrophy was an independent determinant of the contraction duration. The Sm-sigma aft and EF-sigma aft relations at common preloads demonstrated normal contractility in the LVH group. The time constant of the fall in LV pressure and the diastolic myocardial stiffness remained normal in the LVH group. Thus, we introduced the new approach to load-independently assess both the myocardial contractility and the contraction duration in a whole ventricle. A prolonged contraction duration in the presence of normal myocardial contractility was observed in a ventricle with moderate pressure-overload hypertrophy.

Coenzyme Q10 (10 mg/kg/day) or digoxin (2 micrograms/kg/day) was given orally to cardiomyopathic hamsters (BIO 14.6) for 8 weeks from 12 weeks of age. The left ventricular weight per gram of body weight (mg/g) was lower (p less than 0.01) in the coenzyme Q10 group (3.09 +/- 0.13) than in the digoxin (3.32 +/- 0.20) and control (3.44 +/- 0.14) groups. Left ventricular function was evaluated in isovolumically beating hearts. Left ventricular developed pressure (63 +/- 5 vs. 54 +/- 10 mmHg, p less than 0.05), -dP/dt (1385 +/- 100 vs. 1211 +/- 136 mmHg/sec, p less than 0.05), and -dP/dt (1068 +/- 126 vs. 896 +/- 141 mmHg/sec, p less than 0.05) were greater in the coenzyme Q10 than in the control group. The time constant of left ventricular relaxation was shorter in the coenzyme Q10 group than in the control group (25 +/- 3 vs. 28 +/- 3 msec, p less than 0.05). By contrast, in the digoxin group, the indices of left ventricular function did not differ from the control group. These results suggest that coenzyme Q10, but not digoxin, attenuated disease progression and preserved left ventricular function in cardiomyopathic hamsters.

We analyzed the relationships among parameters of left ventricular (LV) early diastolic filling flow (EDF) obtained with pulsed Doppler echocardiography, mean pulmonary wedge pressure (PCWP) and the time constant of LV pressure fall calculated by either Weiss' (Tw) or Thompson's (Tb) method. PCWP correlated with the peak velocity (R) (r = 0.537, p less than 0.05), acceleration (Ac) (r = 0.545, p less than 0.05) and deceleration (Dc) (r = 0.606, p less than 0.01) of LVEDF. In contrast, Tb correlated only with the time to the peak of LVEDF (TPF) (r = 0.487, p less than 0.05), and Tw did not correlate with the Doppler-derived indices significantly. After correcting for the effect of PCWP, significant partial correlations between R and Tw (r = -0.535, p less than 0.05), and between Ac and both Tw (r = -0.606, p less than 0.01) and Tb (r = -0.569, p less than 0.05) were found. Dc did not correlate with Tw or Tb. These results suggest that the level of left atrial pressure may mask the relationship between parameters of LVEDF and LV relaxation, and that the relations among these variables vary with individual indices of LVEDF.

Prognosis of 36 patients with congestive cardiomyopathy was studied in relation to various clinical factors. Half life of the survival curve after overt heart failure was about 7 years. Although left ventricular function was a major determinant of clinical course in congestive cardiomyopathy in general, its relation to prognosis was variable according to the type of cardiac involvement. In peripartal cardiomyopathy and in a type of cardiomyopathy named subacute cardiomyopathy with pulmonary thrombosis in this paper, factor(s) other than left ventricular function, possibly including pulmonary thrombosis, may be operative as more important determinant of extremely poor prognosis in these subtypes. Alcoholic cardiomyopathy was also unique in its favorable prognosis in association with reversible cardiomegaly following abstention from alcohol.

Acute hemodynamic and humoral effects of synthesized alpha human atrial natriuretic polypeptide (alpha-hANP, 0.025 microgram/kg/min for 40 min) on 6 patients with severe congestive heart failure were assessed. Plasma alpha-hANP concentration was high in patients and increased further (from 463 +/- 360 to 1,282 +/- 670 pg/ml, mean +/- SD, p less than 0.01) following alpha-hANP infusion, but plasma norepinephrine (1,030 +/- 865 to 971 +/- 785 pg/ml) was not changed. Increases in urine output (1.0 +/- 0.8 to 2.6 +/- 2.3 ml/min) and Na+ excretion rate (87 +/- 89 to 257 +/- 211 mEq/min/m2) were statistically insignificant. A significant reduction was induced in mean aortic pressure (99 +/- 25 to 96 +/- 26 mmHg, p less than 0.05), mean right atrial pressure (11 +/- 9 to 7 +/- 8 mmHg, p less than 0.01), mean pulmonary arterial pressure (39 +/- 13 to 33 +/- 12 mmHg, p less than 0.05) and mean pulmonary capillary wedge pressure (27 +/- 8 to 20 +/- 7 mmHg, p less than 0.01). Heart rate, cardiac index, systemic vascular resistance and pulmonary vascular resistance were not altered. In conclusion, alpha-hANP induced decreases in left ventricular filling pressure and rightside heart pressure which were attributed to venodilatation rather than natriuresis in patients with congestive heart failure. Preserved cardiac output with decreased preload suggested that alpha-hANP improved cardiac function.

Chronic effects of coenzyme Q10 (CoQ: 30 mg/kg/day for 12 weeks) on cardiac performance in streptozotocin (45 mg/kg) induced diabetic rats were examined. Cardiac performance was assessed using the isolated retrograde perfused isovolumically contracting heart model. Compared to age matched nondiabetic rats, decreases occurred in myocardial CoQ (25.8 +/- 3.3 vs. 31.9 +/- 2.7 micrograms/ml), AMP (0.9 +/- 0.7 vs. 2.0 +/- 0.4 micrograms/mg), Emax (37 +/- 14 vs. 80 +/- 38 mmHg/microliter/g), an index of myocardial contractility, and LV diastolic chamber stiffness constant k (0.68 +/- 0.13 vs. 1.31 +/- 0.59 g/microliter) in diabetic rats. Normalized left ventricular weight (2.97 +/- 0.23 vs. 2.51 +/- 0.21 mg/g) and volume (1.53 +/- 0.34 vs. 0.89 +/- 0.53 microliter/g) and time constant of left ventricular pressure fall, T (32.0 +/- 8.0 vs. 19.7 +/- 2.6 ms) increased in diabetes. In diabetic rats taking CoQ, myocardial CoQ (28.5 +/- 3.2 micrograms/ml) and AMP (2.1 +/- 1.7 micrograms/mg) were the same as control, and T (23.5 +/- 7.4 ms) was significantly shortened (mean +/- SD, p less than 0.05, p less than 0.01). To compensate for depressed myocardial contractility and relaxation, LV dilatation and increased LV mass occurred in diabetic rats. Exogenous CoQ increased myocardial CoQ content and improved myocardial relaxation in diabetic rats.

In a 28-year-old woman with aortitis syndrome, repeated aortography revealed the development of a coarctation of the abdominal aorta occurring over a period of 1 year. Clinical and surgical examinations showed evidence of inflammation and ruled out other diseases during that time. This suggests that in cases of aortitis syndrome arterial lesions may show rapid progression over short time periods and in the absence of untoward events.

Long-term clinical effects of beta-blockers (propranolol in most cases) and calcium inhibitors (nifedipine in most cases) were studied in 16 patients with hypertrophic cardiomyopathy. On overall subjective symptoms, beta-blockers were effective in 50% of symptomatic patients, while calcium inhibitors were effective in only 33%. On angina pectoris, however, calcium inhibitors were superior to beta-blockers in our patients. Blood pressure decreased with each drug, and the decrease was significant with nifedipine. Otherwise there was no change in physical findings with either drug. Long-term (more than 6 months) use of beta-blockers resulted in an increase in cardiothoracic ratio on chest X-ray, a decrease in left ventricular ejection fraction on echocardiogram and more pronounced ST-T change on electrocardiogram. Prolonged use of nifedipine resulted in a slight decrease in cardiothoracic ratio, but no systematic change on echocardiogram and on electrocardiogram.

We studied the effect of alpha human atrial natriuretic polypeptide (hANP) on venous vessels by occlusion plethysmography in 7 patients with congestive heart failure. In another 8 patients the effect of nitroglycerin was studied to validate the methodology. Forearm venous pressure (VP) and volume change (delta V) were measured simultaneously. The relationship between venous pressure and volume change was described by the equation VP = C x e(K x delta V) (r = 0.98 +/- 0.01) and the venous stiffness constant (K) was calculated. Alpha human atrial natriuretic polypeptide (0.1 microM/kg/min) was infused intravenously at a dose sufficient to cause arteriodilation. The pressure-volume curve of the peripheral veins was shifted rightward on the volume axis and the stiffness constant (K) was decreased (-28.1%, p less than 0.03) significantly by nitroglycerin. Alpha human atrial natriuretic polypeptide significantly decreased systemic vascular resistance but did not shift the pressure-volume curve of the vein nor did it decrease the stiffness constant (K). We conclude that hANP has far less venodilating effect than arteriodilating effect in congestive heart failure patients.

Modulation of intracellular Ca2+ concentration [( Ca2+]i) is a signal for the contraction of vascular smooth muscle cells responding to vasoreactive substances. We prepared confluently cultured smooth muscle cells from rat aorta, loaded them with Ca2+ sensitive fluorescent dye, fura-2, and measured the [Ca2+]i transient by microscopic spectrofluorometry. The [Ca2+]i was distributed heterogeneously in cytosol. Angiotensin II (10 nM) transiently doubled the [Ca2+]i. It was also increased by arginine-vasopressin (10 nM), even after stimulation by angiotensin II was saturated. In contrast, acetylcholine (10 microM) or rat atrionatriuretic peptide (10 nM) did not change the [Ca2+]i in the same detecting field of the same cell, contradicting previous reports.

Acute hemodynamic changes induced by two beta-blocking agents, bunitrolol and propranolol, in patients with ischemic heart disease were studied. Besides possessing negative chronotropic and inotropic effects which were demonstrated by decreased heart rate (HR), cardiac index (CI) and double product (DP) of the heart, propranolol significantly increased systemic vascular resistance (SVR, 12%, p less than 0.05) and the time constant of left ventricular (LV) isovolumic pressure fall (T, 10%, p less than 0.01). With bunitrolol, no significant changes were observed in indexes reflecting chronotropic and inotropic states of the heart, and CI and DP were essentially unchanged. Only LV systolic pressure (-5%, p less than 0.01), LV end-diastolic pressure (EDP, -17%, p less than 0.01) and T (-10%, p less than 0.05) decreased significantly. Systemic vascular resistance (SVR) decreased, though insignificantly. Myocardial oxygen supply-demand balance in the resting state was not improved by propranolol as evidenced by the fact that CI decreased in proportion to the decline in DP. In contrast, ischemia at rest was apparently improved by bunitrolol because LV wall stress decreased due to the reduction in LV volume which was suggested by the decline in LV systolic pressure and LVEDP while CI remained constant. Improvement of the time constant T might be strong evidence of relief from ischemia. Bunitrolol might be effective even in patients with overt heart failure, especially that due to ischemic heart disease because of its lack of negative inotropic action and its ameliorating effect on ischemia at rest.