Effects of calcitonin gene-related peptide on cardiac contractility, coronary hemodynamics and myocardial energetics in idiopathic dilated cardiomyopathy.

This study was performed to examine the effects of calcitonin gene-related peptide on cardiac function and coronary circulation in patients with heart failure. Synthetic human calcitonin gene-related peptide was infused in the left main coronary artery of 9 patients undergoing cardiac catheterization at different doses corresponding to incremental infusion rates of 15, 50, 150 and 600 pmol.min-1. No hemodynamic change was observed in response to administration of the 2 lowest doses. The 2 highest doses induced an increase in cardiac index and a decrease in systemic arterial pressure. The infusion of 600 pmol.min-1 resulted in a decrease of mean systemic arterial pressure (86.8 +/- 6.5 to 71.8 +/- 4.9 mm Hg; p less than 0.01), and an increase in both cardiac index (2.1 +/- 0.1 to 3.1 +/- 0.17 liters.min-1.m-2; p less than 0.01) and heart rate (87 +/- 3.7 to 101 +/- 6.1 beats.min-1; p less than 0.01). These hemodynamic changes were associated with a significant increase in plasma norepinephrine and epinephrine concentrations. Peak positive first derivative of left ventricular pressure did not change at any infusion rate. Left ventricular end-diastolic pressure decreased at the 2 highest doses associated with a decrease in plasma atrial natriuretic factor concentration (730 +/- 140 to 436 +/- 115 pg.ml-1; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of sustained isometric handgrip on praecordial accelerocardiogram in normal subjects and in patients with heart disease.

The effects of isometric exercise on the maximum amplitude of the praecordial accelerocardiogram (as represented by the DE deflection) have been compared in 6 normal subjects (group 1), 12 patients with aortic stenosis (group 2), and 16 patients with myocardial disease (group 3). Whereas the tachycardia and pressor effects of isometric exercise were identical in all three groups, the normal subjects showed a significant decrease in DE during handgrip of 10 +/- 4 per cent (P less than 0.05) as compared with the insignificant increases of 8.5 +/- 6 per cent (P greater than 0.5), and 4 +/- 3.5 per cent (P greater 0.3) observed in the patients in groups 2 and 3. This response in the normal subjects differed significantly from the responses observed in the patients in groups 2 (P less than 0.02) and 3 (P less than 0.01). Of the patients in each of groups 2 and 3, 50 per cent responded abnormally to handgrip in that they showed a significant increase in DE. In the patients with aortic stenosis this subgroup of patients differed from the remainder in that they had a higher resting cardiac index (P less than 0.05). In the patients with myocardial disease this subgroup was characterized by a significantly lower resting left ventricular end-diastolic pressure (P less than 0.02). It seems, therefore, that those patients who increase DE in response to handgrip tend to have better left ventricular function at rest than those who do not. We suggest that this may be because of increased beta adrenergic activity at rest and during isometric exercise in the subgroup who respond to handgrip with an increase in DE.     

Effects of sustained isometric handgrip on praecordial accelerocardiogram in normal subjects and in patients with heart disease.

The effects of isometric exercise on the maximum amplitude of the praecordial accelerocardiogram (as represented by the DE deflection) have been compared in 6 normal subjects (group 1), 12 patients with aortic stenosis (group 2), and 16 patients with myocardial disease (group 3). Whereas the tachycardia and pressor effects of isometric exercise were identical in all three groups, the normal subjects showed a significant decrease in DE during handgrip of 10 +/- 4 per cent (P less than 0.05) as compared with the insignificant increases of 8.5 +/- 6 per cent (P greater than 0.5), and 4 +/- 3.5 per cent (P greater 0.3) observed in the patients in groups 2 and 3. This response in the normal subjects differed significantly from the responses observed in the patients in groups 2 (P less than 0.02) and 3 (P less than 0.01). Of the patients in each of groups 2 and 3, 50 per cent responded abnormally to handgrip in that they showed a significant increase in DE. In the patients with aortic stenosis this subgroup of patients differed from the remainder in that they had a higher resting cardiac index (P less than 0.05). In the patients with myocardial disease this subgroup was characterized by a significantly lower resting left ventricular end-diastolic pressure (P less than 0.02). It seems, therefore, that those patients who increase DE in response to handgrip tend to have better left ventricular function at rest than those who do not. We suggest that this may be because of increased beta adrenergic activity at rest and during isometric exercise in the subgroup who respond to handgrip with an increase in DE.     

Hemorrhagic shock depresses myocardial contractile function in the guinea pig

Isolated coronary-perfused guinea pig hearts were used to determine if in vivo hemorrhagic shock (mean arterial blood pressure, 32.8 +/- 2.3 mmHg for 2 hr) alters intrinsic contractile function of the left ventricle. Compared to control hearts, shocked hearts developed significantly less left ventricular pressure (control: 64.7 +/- 3.3; shock: 34.1 +/- 3.1 mmHg, P less than .001) and +dP/dt max (control: 1,429 +/- 187; shock: 894 +/- 119 mmHg/sec, P less than .038) and -dP/dt max (control: 1,416 +/- 176; shock: 808 +/- 94 mmHg/sec, P less than .011) at a left ventricular end-diastolic pressure of 10 mmHg. Increasing left ventricular end-diastolic pressure from 0 to 20 mmHg, electrical pacing at control heart rate, and increased coronary flow rate failed to restore shock-induced cardiac dysfunction. Left ventricular function curves calculated from shocked hearts were shifted downward and to the right of values obtained from control hearts (P = .001). Furthermore, left ventricular performance in shocked hearts remained depressed as extracellular calcium concentration was increased from 1 to 8 mM. While calcium increased left ventricular pressure, +dP/dt max, and -dP/dt max in a dose-dependent manner in both control and shocked hearts, all indices of contractile performance were consistently less in shocked hearts than those measured in control hearts at each calcium concentration. Our data suggest that cardiac depression is a feature of hemorrhagic shock.     

Nisoldipine improves blood flow to skeletal muscles in conscious pigs with chronic heart failure

We studied the acute effects of the calcium antagonist nisoldipine in 10 conscious pigs with chronic heart failure. Left ventricular dysfunction was induced by permanent ligation of the left circumflex coronary artery. Two to three weeks after myocardial infarction the effects of four consecutive 10 min intravenous infusions of nisoldipine (0.05; 0.1; 0.25 and 0.5 micrograms kg-1 min-1) or its solvent on systemic haemodynamics were evaluated. In addition, we used the radioactive microsphere technique to study the distribution of cardiac output after each dose of nisoldipine. Nisoldipine significantly (P less than 0.05) increased heart rate (from 144 +/- 9 to 161 +/- 8 beats min-1), cardiac output (from 2.1 +/- 0.1 to 2.9 +/- 0.2 l min-1), stroke volume (from 14 +/- 1 to 18 +/- 1 ml) and left ventricular dP/dtmax (from 2600 +/- 100 to 3500 +/- 250 mmHg s-1), but had no effect on arterial blood pressure. Left ventricular end-diastolic pressure (from 19 +/- 2 to 16 +/- 1 mmHg) and systemic vascular resistance (from 52 +/- 3 to 37 +/- 3 mmHg min l-1) decreased after nisoldipine. The nisoldipine-induced increase in cardiac output did not affect blood flow to the kidneys, brain, liver or skin, but perfusion of the stomach (84%), adrenals (84%) and normal myocardium (from 200 +/- 25 to 321 +/- 38 ml min-1 100 g-1) as well as infarcted myocardium (from 41 +/- 8 to 61 +/- 19 ml min-1 100 g-1) increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Additive effects of enoximone and nitroprusside in unstable chronic heart failure

In the present study, the safety and efficacy of the combined administration of intravenous nitroprusside and oral enoximone, an experimental compound with phosphodiesterase inhibitory properties, were evaluated. Ten patients with unstable chronic heart failure maintained on digitalis and diuretics were selected to receive enoximone because of their poor response to intravenous nitroprusside. For a mean peak dose of 115 micrograms min-1 nitroprusside, cardiac index increased from 1.8 +/- 0.4 to 2.0 +/- 0.4 l min-1 m-2, while pulmonary artery diastolic pressure and mean right atrial pressure decreased from 29 +/- 6 to 24 +/- 5 and from 15 +/- 6 to 11 +/- 3 mmHg respectively; mean arterial pressure and heart rate were unchanged. The addition of 1.6 mg kg-1 oral enoximone t.i.d. to nitroprusside resulted in a substantial improvement of cardiac function: cardiac index increased further to 2.8 +/- 0.5 l min-1 m-2 (P less than 0.001), pulmonary artery diastolic pressure and right atrial pressure decreased to 18 +/- 5 and 7 +/- 3 mmHg (P less than 0.01), respectively, while mean arterial pressure rose from 90 +/- 11 mmHg to 95 +/- 0 mmHg (P less than 0.05); heart rate was unchanged. The salutary haemodynamic response to combined nitroprusside-enoximone therapy persisted for more than 32 h, and cardiac performance remained improved on enoximone for a further 8 h despite the discontinuation of nitroprusside. No serious side-effects or changes in the arrhythmia profile were observed. The addition of oral enoximone to nitroprusside has beneficial haemodynamic effects in unstable chronic heart failure.     

Demonstration of dissimilar acute haemodynamic effects of ethanol and acetaldehyde.

To determine whether the acute cardiac depressant effects of ethanol could be attributed to its metabolite (acetaldehyde), either ethanol or acetaldehyde was intravenously infused into pentobarbital anaesthetised, closed-chest dogs. At a venous blood ethanol level of 199 +/- 43 (SE) mg . dl-1, ejection fraction had decreased from 35 +/- 2 to 30 +/-2%, P less than 0.05, max dP/dt/end-diastolic volume from 14.0 +/- 2.1 to 8.6 +/- 1.1 kPa . s-1 . cm-3 (105 +/- 16 to 65 +/- 8 mmHg . s-1 . cm-3), P less than 0.02, whereas end-diastolic volume (P less than 0.005), myocardial oxygen consumption (P less than 0.05) and coronary blood flow (P less than 0.005) had increased. Higher ethanol levels exaggerated these changes when peak arterial acetaldehyde was 20.2 +/- mumol . litre-1. By contrast, infusion of acetaldehyde to a peak blood level comparable with that produced by ethanol increased cardiac output from 2.4 +/- 0.2 to 2.8 +/- 0.2 litre-1 . min-1 P less than 0.01), coronary sinus oxygen saturation from 46 +/- 4 to 55 +/- 3% (P less than 0.25) and reduced systemic resistance from 8.0 +/- 0.7 to 6.3 +/- 0.5 kPa . litre-1 . min-1 (60 +/- 5 to 47 +/- 4 mmHg . litre-1 . min-1) (P less than 0.001). High dosage of acetaldehyde to a level of 129 +/- 23 mumol . litre-1 produced elevation of cardiac output (P less than 0.001), ejection fraction (P less than 0.01), coronary blood flow (P less than 0.02), whereas systemic resistance (P less than 0.001), heart rate (P less than 0.05) and myocardial oxygen consumption (P less than 0.05) decreased. Discontinuation of acetaldehyde infusion significantly reversed these changes. Max dP/dt/left ventricular end-diastolic volume and left ventricular end-diastolic volume were not significantly altered by acetaldehyde. Thus, ethanol depresses cardiac performance and increases myocardial oxygen consumption. By contrast, acetaldehyde at levels produced by ethanol metabolism improves cardiac performance, consequent to afterload reduction, and reduces myocardial oxygen consumption.     

Correlation between praecordial accelerocardiogram and left ventricular pressure.

The praecordial accelerocardiogram possesses important practical advantages over more familiar techniques of recording praecordial pulsations. We have compared the amplitude of the P wave of the praecordial accelerocardiogram in 6 normal subjects (group 1) and 21 patients with heart disease (group 2) at rest and after 3 minutes of isometric handgrip at 30 per cent maximum voluntary contraction. At rest in group 2 there was a significant linear correlation between the amplitude of the P wave of the accelerocardiogram, relative to the maximum systolic amplitude (P/DE), and the left ventricular end-diastolic pressure (P less than 0-01). However, comparison of the data for P/DE showed that the mean value (+/-SEM) of 29+/-5 per cent in group 1 was not significantly different from the mean value of 37+/-4 per cent in group 2 (P g .reater than 0-30). During handgrip the mean amplitude of the P wave did not increase significantly in group 1 (P greater than 0-20) but increased significantly in group 2 (P less than 0-02). In group 2 there was a significant linear correlation between the percentage increase in the amplitude of the P wave of the accelerocardiogram during handgrip and the percentage increase in the left ventricular end-diastolic pressure (P less than 0-01).     

Correlation between praecordial accelerocardiogram and left ventricular pressure.

The praecordial accelerocardiogram possesses important practical advantages over more familiar techniques of recording praecordial pulsations. We have compared the amplitude of the P wave of the praecordial accelerocardiogram in 6 normal subjects (group 1) and 21 patients with heart disease (group 2) at rest and after 3 minutes of isometric handgrip at 30 per cent maximum voluntary contraction. At rest in group 2 there was a significant linear correlation between the amplitude of the P wave of the accelerocardiogram, relative to the maximum systolic amplitude (P/DE), and the left ventricular end-diastolic pressure (P less than 0-01). However, comparison of the data for P/DE showed that the mean value (+/-SEM) of 29+/-5 per cent in group 1 was not significantly different from the mean value of 37+/-4 per cent in group 2 (P g .reater than 0-30). During handgrip the mean amplitude of the P wave did not increase significantly in group 1 (P greater than 0-20) but increased significantly in group 2 (P less than 0-02). In group 2 there was a significant linear correlation between the percentage increase in the amplitude of the P wave of the accelerocardiogram during handgrip and the percentage increase in the left ventricular end-diastolic pressure (P less than 0-01).     

Haemodynamics of induced atrial fibrillation: a comparative assessment with sinus rhythm, atrial and ventricular pacing

The haemodynamics and myocardial lactate consumption during induced atrial fibrillation (AF) were studied in 10 patients with paroxysmal AF. Their mean age (+/- SD) was 61 +/- 5 years and none had clinical evidence of ischaemic or rheumatic heart disease. Compared with sinus rhythm, the onset of AF was associated with a reduction in systolic blood pressure (152 +/- 13 mmHg) in AF vs 169 +/- 23 mmHg in sinus rhythm, P less than 0.01). There was no consistent change in cardiac output at the onset of AF compared with sinus rhythm, but the cardiac output was lower compared with regular atrial pacing at rates similar to those of induced AF (3.85 +/- 0.76 vs 4.38 +/- 0.89 l min-1, P less than 0.02). Compared with sinus rhythm or rate-matched atrial pacing, AF was associated with an elevated pulmonary arterial pressure (24.2 +/- 5.6 mmHg in AF vs 17.9 +/- 14.4 mmHg in sinus rhythm, P less than 0.01) and pulmonary arterial wedge pressure (18.6 +/- 5.6 vs 9.7 +/- 3.9 mmHg, P less than 0.01). The haemodynamic changes during AF were similar to those seen during regular ventricular pacing at an equivalent rate, although the latter was associated with a lower systolic blood pressure (152 +/- 13 mmHg in AF vs 136 +/- 25 mmHg in ventricular pacing, P less than 0.05) and higher right atrial pressure (8.2 +/- 4.4 vs 11.5 +/- 7.5 mmHg respectively, P less than 0.05), presumably due to the deleterious effects of cannon 'a' waves.(ABSTRACT TRUNCATED AT 250 WORDS)     

Tei-index in patients with mild-to-moderate congestive heart failure.

BACKGROUND: Congestive heart failure is related to contraction and relaxation abnormalities of the ventricle. Isolated analysis of either mechanism may not be reflective of overall cardiac dysfunction. A combined myocardial performance index (isovolumic contraction time plus isovolumic relaxation time divided by ejection time, 'Tei-Index') has been described which may be more effective for analysis of global cardiac dysfunction than systolic and diastolic measures alone. It was the aim of the present investigation to evaluate the Tei-Index against invasive examination. METHODS AND RESULTS: Eighty-one subjects were included in a consecutive manner, among 125 patients undergoing left heart catheterization for invasive measurement of left ventricular end-diastolic pressure; 43 patients had congestive heart failure (35 male, 8 female, 68+/-6 years) defined by NYHA functional class >/=2 (mean 2.5+/-0.5) and left ventricular end-diastolic pressure >/=16 mmHg (mean 20+/-4) and 38 subjects (32 male, 6 female, 66+/-5 years) without symptoms of heart failure (NYHA functional class I) and with normal left ventricular end-diastolic pressure (mean 12+/-3 mmHg) served as a control group. Using conventional echo-Doppler methods, parameters assessed were: ejection fraction, peak velocities of early (E) and late (A) diastolic filling, the E/A ratio, deceleration time, isovolumic contraction time, isovolumic relaxation time and ejection time. The Tei-Index was obtained by subtracting ejection time from the interval between cessation and onset of the mitral flow. The control group and patients with congestive heart failure did not differ with respect to the E/A ratio (0.86+/-0.27 vs 0.90+/-0.44, P=ns), deceleration time (203+/-42 ms vs 206+/-36 ms, P=ns) and isovolumic relaxation time (97+/-16 ms vs 94+/-26 ms, P=ns). The ejection fraction was slightly reduced in patients with congestive heart failure (46+/-11% vs 55+/-8%, P<0.05). The Tei-Index was easily and reproducibly measured in all subjects. The mean value of the Tei-Index was significantly different between the control group and patients with congestive heart failure (0.39+/-0.10 vs 0.60+/-0.18, P<0.001). Receiver operating characteristic curve analysis for the Tei-Index yielded an area under the curve of 0.88+/-0.038. Using a Tei-Index >/=0.47 as the cutpoint, congestive heart failure was identified with a sensitivity of 86% and a specificity of 82%. No correlation was observed between the Tei-Index and heart rate (r=0.22, P=ns), systolic blood pressure (r=0.16, P=ns) or diastolic blood pressure (r=0.08, P=ns). The Tei-Index was significantly related to left ventricular end-diastolic pressure (r=0.46, P<0.01). CONCLUSION: The Tei-Index is a sensitive indicator of overall cardiac dysfunction in patients with mild-to-moderate congestive heart failure. The Tei-Index is easily obtained and may be used in the work-up of patients with suspected cardiac dysfunction.     

The acute effects of intravenous xamoterol ('Corwin', I.C.I. 118, 587) on resting and exercise haemodynamics in patients with mild to moderate heart failure

The known properties of xamoterol, a partial beta 1-agonist, provide a basis to pharmacologically modulate cardiac responses to variations in sympathetic tone. Haemodynamic variables were assessed at rest and on exercise before and after intravenous xamoterol (0.2 mg kg-1), in 30 patients with mild to moderate cardiac failure. Xamoterol produced significant improvements in resting cardiac index (2.51 +/- 0.15 to 2.80 +/- 0.14 l min-1 m-2; P less than 0.001), stroke volume (62 +/- 4 to 75 +/- 5 mljbeat-1; P less than 0.001) and stroke work index (42.4 +/- 3.6 to 47.7 +/- 3.9 gm beat-1 m-2; P less than 0.01). This occurred despite a significant reduction in heart rate (78 +/- 3 to 74 +/- 2 beats min-1; P less than 0.05). There were also significant reductions in systemic vascular resistance (1990 +/- 141 to 1669 +/- 112 dynes s-1 cm-5; P less than 0.01) and double product (1146 +/- 46 to 1051 +/- 41 mmHg min-1 x 10(-1); P less than 0.05), with no significant changes in systolic blood pressure, pulmonary wedge pressure or ejection fraction. Xamoterol significantly attenuated the heart rate response to exercise (112 +/- 4 to 97 +/- 3 beats min-1; P less than 0.001), with no impairment in the expected exercise induced increase in cardiac index. This was due to the significant increase in stroke volume from 81 +/- 6 to 95 +/- 7 ml beat-1 (P less than 0.001). There were no significant changes in resting or exercise noradrenaline levels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute effects of alcohol on left ventricular dynamics during isometric exercise in normal subjects

The aim of this study was to assess whether drinking social amounts of alcohol impairs myocardial contractility in normal humans. To that end, 17 healthy volunteers performed isometric handgrip exercise before and 60 minutes after an intake of 1 g/kg body weight of ethanol within 60 minutes. Left ventricular M-mode echocardiogram, systolic time intervals, and sphygmomanometric arterial blood pressure were recorded before and at the end of 4-min handgrip at 30% of maximum voluntary contraction. The blood ethanol concentration (mean +/- SD) was 24.4 +/- 2.0 mmol/liter. At rest, ethanol increased heart rate (p less than 0.05), and decreased left ventricular end-diastolic diameter (p less than 0.05), end-systolic diameter (p less than 0.01), and circumferential systolic wall stress (p less than 0.05). The indices of left ventricular performance were unchanged except for the maximum circumferential fiber shortening velocity which was increased after ethanol (p less than 0.001). The cardiac response to isometric exercise was similar before and after ethanol except that the handgrip-induced rise in systolic wall stress was smaller postingestion (p less than 0.05). This study does not support the view that drinking small to moderate amounts of alcohol brings about myocardial depression in normal humans. Although preload, afterload, and heart rate were altered by ethanol at rest, myocardial contractility was not impaired even during the afterload stress imposed by isometric exercise.     

Cardiac performance in rats with renal hypertension.

To evaluate cardiac performance in renal hypertension more precisely we determined cardiac function curves for 12 normotensive rats and 11 other rats with two-kidney Goldblatt hypertension. The hypertensive group (BP = 134 +/- 8 mm Hg) showed significant cardiac hypertrophy (44 +/- 1% increased ratio of heart weight to body weight, P less than 0.01) and markedly increased left ventricular stroke work with a moderate but not significant increase in left ventricular end-diastolic pressure (LVEDP) (5.9 +/- 0.8 vs. 4.7 +/- 0.4 mm Hg). We evaluated cardiac function by recording left ventricular end-diastolic pressure, stroke volume (SV), and cardiac output (CO) (by electromagnetic flowmeter) during rapid alteration in venous return. Analysis of variations of stroke volume vs. left ventricular end-diastolic pressure showed that renal hypertension is accompanied by a significant decrease in ventricular performance [SV = 0.0190 + 0.0509 LVEDP - 0.0025 (LVEDP)2 + 0.0001 (LVEDP)3] compared to the normotensive group [SV = 0.0430 + 0.0644 LVEDP - 0.0040 (LVEDP)2 + 0.001 (LVEDP)3]. The alterations in stroke volume and cardiac output were associated with a lack of significant changes in the work performed at matched end-diastolic pressures. The data indicate that chronic renal hypertension is accompanied by a depression of cardiac reserve which is not revealed by measurements of cardiac output and left ventricular end-diastolic pressure at rest. This impairment in cardiac function might be related to either diminished cardiac contractility or reduced left ventricular compliance; the latter possibility is in accord with our finding of a 2-fold increase in the hydroxyproline content (P less than 0.001) and a significant decrease in the DNA concentration of ventricular tissue.     

Hemodynamic response to isometric exercise in elderly subjects

The haemodynamic responses to isometric exercise (handgrip) performed during right cardiac catheterization were tested in 9 elderly patients (1 female, 8 males) with average age of 67.8 +/- 2.3 years, without clinical and instrumental signs of cardiovascular disease. The parameters tested before and after handgrip were: heart rate (FC), systolic blood pressure (PAS), diastolic blood pressure (PAD), mean blood pressure (PAM), cardiac output (PC), cardiac index (IC), systolic index (IS), mean pulmonary pressure (PPM), end-diastolic pulmonary pressure (PPTD), systemic arterial resistance (RST), pulmonary arterial resistance (RPT), stroke volume (GS), left ventricular systolic stress index (ILS). Statistical analysis was carried out using the Student test. Stress produced a highly significant increase (p less than 0.001) of PPM (+28%) of PPTD (+ 33.1%), a modestly significant increase (p less than 0.01) of PAD (+ 15.6%), PAM (+ 18.2%), ILS (+ 24%,), RPT (+ 25%), a weakly significant increase (p less than 0.05) of PAS (+ 20%), RST (+ 15.6%). No significant variation attributable to FC, IC, IS, GS was observed. Our subjects presented a reduced tolerance to isometric exercise.     

Effect of xamoterol on myocardial energetics in man

We analyzed the effect of xamoterol (beta 1-partial agonist) on myocardial energetics in 8 patients with normal left ventricular function. We measured resting systemic and coronary hemodynamics before and after a single intravenous injection of xamoterol (0.1 mg/kg). This agent increased heart rate from 70 +/- 7 to 80 +/- 11 beats/min (p less than 0.05) and cardiac index from 2.9 +/- 0.5 to 3.2 +/- 0.5 L/min.m2 (p less than 0.01), respectively. Left ventricular peak positive dp/dt (1870 +/- 350 vs 2620 +/- 580 mmHg/sec (p less than 0.01) and left ventricular ejection fraction (62 +/- 7 vs 70 +/- 7% (p less than 0.01] also increased, while left ventricular end-diastolic pressure (9 +/- 3 vs 5 +/- 3 mmHg (p less than 0.01] and volume index (70 +/- 14 vs 58 +/- 16 ml/m2 (p less than 0.01] decreased. Coronary blood flow and total myocardial oxygen consumption did not change significantly after intervention. As a result, xamoterol enhanced left ventricular external mechanical work versus myocardial oxygen consumption ratio (mechanical efficiency) from 20 +/- 4 to 24 +/- 5% (p less than 0.01). Myocardial oxygen extraction ratio decreased significantly (p less than 0.01) from 66 +/- 5 to 62 +/- 5% after xamoterol. We conclude that xamoterol augments left ventricular mechanical efficiency accompanied by a decrease in coronary vascular tone in patients with normal cardiac function.     

Effect of ibopamine on the failing heart at rest and during isometric exercise: a noninvasive study

Eleven patients suffering from heart failure were treated with oral ibopamine, a di-isobutyric ester of N-methyldopamine, 100 mg three times a day for 1 week and 200 mg three times a day for 3 weeks. Therapy was discontinued by one patient because of tachycardia. Left ventricular performance was evaluated with echocardiography and systolic time intervals at rest and after 3 minutes of isometric exercise using a handgrip. Six of 10 patients completing the study were in New York Heart Association (NYHA) functional class III, 2 in class IV, and 2 in class II. All patients, except one who remained stable in class II, improved their subjective condition by one functional class during 4 weeks of therapy (p less than 0.01). There were no changes in heart rate, blood pressure, rate-pressure product, cardiac index, or total peripheral vascular resistance. The left ventricular end-systolic diameter decreased after four weeks from 71.2 +/- 12.7 (SD) to 65.9 +/- 13.0 mm (p less than 0.001); the left ventricular end-diastolic diameter did not change. The ejection fraction increased from 26 +/- 8 to 32 +/- 9% (p less than 0.01). Afterload, that is, left ventricular circumferential systolic wall stress, declined as a result of decreased systolic diameter. Systolic time intervals did not vary. There were no changes due to ibopamine during isometric exercise probably owing to increased beta-adrenergic stimulation induced by the handgrip. Neither urine volume nor body weight changed. Side effects were mild except for tachycardia of one patient.(ABSTRACT TRUNCATED AT 250 WORDS)     

Portal vein pulsatility index is a more important indicator than congestion index in the clinical evaluation of right heart function

AIM: To study the changes of portal blood flow in congestive heart failure. METHODS: We studied the congestion index (CI) and portal vein pulsatility index (PI) in patients with varied degrees of congestive heart failure using ultrasonic Doppler. Ten patients with (mean) right atrial pressure (RA) < 10 mmHg were classified as group 1 and the remaining 10 patients with RA > or = 10 mmHg as group 2. RESULTS: There were no difference on cardiac index (HI, P=0.28), aortic pressure (AO, P=0.78), left ventricular end-diastolic pressure (LVED, P=0.06), (max)imum portal blood velocity (Vmax, P=0.17), (mean) portal blood velocity (Vmean, P=0.15) and portal blood flow volume (PBF, P=0.95) between the two groups. Group 2 patients had higher pulmonary wedge pressure (PW, 29.9+/-9.3 mmHg vs 14.6+/-7.3 mmHg, P=0.002), pulmonary arterial pressure (PA, 46.3+/-13.2 mmHg vs 25.0+/-8.2 mmHg, P=0.004), RA (17.5+/-5.7 mmHg vs 4.7+/-2.4 mmHg, P<0.001), right ventricular end-diastolic pressure (RVED, 18.3+/-5.6 mmHg vs 6.4+/-2.7 mmHg, P<0.001), CI (8.7+/-2.4 vs 5.8+/-1.2, P=0.03), and PI (87.8+/-32.3% vs 27.0+/-7.4%, P<0.001) than Group 1. CI was correlated with PI (P<0.001), PW (P<0.001), PA (P<0.001), RA (P=0.043), RVED (P=0.005), HI (P<0.001), AO (P<0.001), CO (P<0.001), LVED (P<0.001), Vmax (P<0.001), Vmean (P<0.001), cross-sectional area of the main portal vein (P<0.001) and PBF (P<0.001). CI could be as high as 8.3 in patients with RA < 10 mmHg and as low as 5.9 in those with RA > or = 10 mmHg. CONCLUSION: Our data show that RI is a more significant indicator than CI in the clinical evaluation of high RA > or = 10 mmHg, whereas CI is better than PI in the assessment of left heart function.     

Short-term haemodynamic evolution and late follow-up of post-infarct patients with left ventricular dysfunction undergoing a physical training programme

The aims of this study were to investigate the short-term haemodynamic changes occurring in post-infarct patients with left ventricular dysfunction undergoing a physical training programme and the prognostic implications of such changes. Ninety-five male patients with no evidence of congestive heart failure, consecutively admitted for exercise testing with haemodynamic monitoring in the supine position, in whom exercise pulmonary artery diastolic pressure (PAdP) exceeded 20 mmHg were enrolled in an in-hospital one-month physical training programme. After training all patients' exercise capacity increased by 24% (P less than 0.001) with no change of PAdP. At matched work load, heart rate decreased (126 +/- 21 vs 120 +/- 19 bt min-1, P less than 0.05) as did PAdP (27 +/- 5 vs 25 +/- 6 mmHg, P less than 0.05) and A-VO2 difference increased (9.5 +/- 1.7 vs 10 +/- 1.6 ml%, P less than 0.01). Similar results were observed in a subset of patients with exercise PAdP greater than 30 mmHg (30 patients). In 11 patients with inadequate cardiac output neither heart rate nor PAdP decreased after training and a disproportionate increase in blood pressure was noted. Clinical follow-up ranged from 1 to 8 years (62 +/- 32 months). Seven deaths, 12 reinfarctions and 14 coronary artery bypass graftings occurred. The modifications, after training in work capacity, heart rate and PAdP, were not predictive of events.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative study of iohexol and iopamidol as cardioangiographic contrast media

We have done a double-blind randomized study to compare the cardiac effects of 2 nonionic low osmolality contrast agents, iohexol (n = 25) and iopamidol (n = 25), for left ventriculography and coronary arteriography. No statistical differences were detected between both groups in quality of image, clinical (absence of nausea; intense warmth [8% vs 8%, p = NS]) and electrocardiography (repolarization changes [24% vs 12%, p = NS], absence of severe bradycardia and ventricular arrhythmia) effects. Ventriculography induced no change in systolic left ventricular pressure (iohexol: 128.6 +/- 18 vs 127 +/- 19 mmHg, p = NS; iopamidol: 133 +/- 24 vs 131.8 +/- 23 mmHg, p = NS), and a little but significant rise in left ventricular end-diastolic pressure (iohexol: pre = 11.6 +/- 7 vs post = 13.9 +/- 7 mmHg, p less than 0.01; iopamidol: 11.7 +/- 4 vs post = 15.5 +/- 5 mmHg, p less than 0.001). Our results suggest that iohexol and iopamidol are comparable and qualified for angiocardiography.