Biomedical subjects

H Just

Publications and source records attributed to H Just.

At least 181 records · Page 10Linked to original sources

PubMed1991

[Tachycardic arrhythmias in athletes. Incidence, clinical relevance and prognostic significance].

Morphological and functional cardiac changes are found in all active athletes. Of particular interest would appear to be tachycardic arrhythmias, since they have been associated with cases of sudden death during sports activities. In comparison with patients with underlying cardiac disease, few data on the incidence and prognostic significance of tachycardic arrhythmias in athletes are available. The aim of the present study was to characterize and identify prognostically relevant tachycardic arrhythmias in this latter population.

Death, Sudden↗

PubMed1991

Assessment of coronary vasomotor tone in humans.

The assessment of endothelium-mediated modulation of coronary vasomotor tone in the intact human circulation under physiologic conditions requires very precise determination of both epicardial artery diameters, reflecting effects within the conduit vessels, as well as coronary blood flow, reflecting effects within the resistance vasculature during cardiac catheterization. In the present report, the accuracy and limitations of quantitative approaches to assess arterial dimensions from coronary angiograms are discussed. Using state-of-the-art image-processing techniques and x-ray imaging, epicardial artery diameter changes within the range of 8-10% can be reliably detected by quantitative coronary angiography. In addition, advances in interventional techniques do provide a means to selectively assess intracoronary blood-flow velocities using intracoronary Doppler catheters. Combining epicardial artery diameter measurements and intracoronary blood-flow velocity parameters allows for a reasonably accurate instantaneous estimate of coronary arterial blood flow. The advantages and limitations of the intracoronary Doppler technique compared to other techniques are discussed.

Coronary Angiography↗

PubMed1991

QT-interval prolonging drugs: mechanisms and clinical relevance of their arrhythmogenic hazards.

The antiarrhythmic principle of drug-induced QT-interval prolongation is well known. However, with the widespread use of the presently known and new Class III antiarrhythmic agents under investigation, and the growing number of agents not primarily designed as antiarrhythmic drugs that potentially cause QT prolongation, we have also become aware of the proarrhythmic hazards associated with many of these agents. The proarrhythmic risk differs markedly from one agent to another and interferes with many individual clinical variables (e.g., hypokalemia, sinus bradycardia). This paper summarizes the present data on the proarrhythmic risk of drug-induced QT prolongation, including the value and problems of the rate-corrected QT interval, the mechanisms involved in the genesis of proarrhythmia, and the clinical cofactors that facilitate the occurrence of proarrhythmic events. In addition, an extensive database provides information on the known proarrhythmic risk of all currently used QT-prolonging agents.

Animals↗

PubMed1991

Electrocardiographic and antiarrhythmic effects of intravenous amiodarone: results of a prospective, placebo-controlled study.

The antiarrhythmic efficacy of intravenously administered amiodarone was examined in a prospective, randomized, placebo-controlled study that involved 77 patients after coronary artery bypass surgery. Amiodarone was given after surgery in a loading bolus of 300 mg for 2 hours followed by 1200 mg every 24 hours for 2 days and 900 mg every 24 hours for the next 2 days. Amiodarone suppressed both supraventricular and ventricular arrhythmias within 12 hours after the start of therapy. Particularly, the incidence of atrial fibrillation (5% vs 21% in the control group; p less than 0.05) and of nonsustained ventricular tachycardia (3% vs 16%; p less than 0.05) was reduced by amiodarone. Heart rate was slowed (p less than 0.001) and repolarization--as judged by JTc interval--was prolonged compared with the control group (p less than 0.01). In two patients, amiodarone infusion was stopped because of excessive QTc prolongation. No detrimental hemodynamic effects of the drug were observed. Thus the intravenous administration of amiodarone appears to be suitable for patients in whom rapid suppression of symptomatic supraventricular and ventricular arrhythmias is warranted in the presence of left ventricular dysfunction.

Aged↗

PubMed1991

Assessment of coronary artery patency after thrombolytic therapy: accurate prediction utilizing the combined analysis of three noninvasive markers.

The predictability of patency of the infarct-related artery assessed by means of three noninvasive easily obtainable markers was prospectively examined in 82 patients undergoing thrombolysis for their first myocardial infarction. Positive noninvasive markers were defined as follows: 1) early peak creatine kinase (CK) activity less than or equal to 12 h after the start of thrombolysis; 2) greater than or equal to 50% reduction in ST segment elevation; and 3) occurrence of reperfusion arrhythmias within the 1st 90 min of thrombolytic therapy. In 63 (77%) of the 82 patients, Thrombolysis in Myocardial Infarction (TIMI) grade II/III reperfusion was achieved within the 1st 90 min as assessed by coronary angiography. Separate analysis of each marker revealed the following respective values for sensitivity, specificity and positive and negative predictive value regarding prediction of coronary artery patency: CK peak less than or equal to 12 h: 84%, 95%, 98% and 64%; reduction of the ST segment elevation greater than or equal to 50%: 60%, 95%, 97% and 42%; and reperfusion arrhythmias: 63%, 89%, 95% and 43%. The combined analysis of all three markers utilizing a logistic regression procedure showed that CK peak (p = 0.0001) and resolution of the ST segment elevation (p = 0.005), but not the occurrence of reperfusion arrhythmias (p = 0.26), were independent predictors of vessel patency. From this logistic regression procedure, a sensitivity of 100%, a specificity of 90%, a positive predictive value of 97% and a negative predictive value of 100% for prediction of coronary artery patency were obtained.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗

PubMed1991

Efficacy and tolerance of the new class IB antiarrhythmic barucainide: an intravenous dose-finding study.

Barucainide is a new class IB antiarrhythmic agent that was studied for efficacy and safety after intravenous administration in patients with severe ventricular arrhythmias. All patients received 80 mg/hr barucainide intravenously for 7 hours or until ventricular arrhythmias were suppressed by greater than 90%. In responders a maintenance dose was given for 24 hours, aimed to achieve steady-state conditions. At baseline and during the treatment and washout periods 24-hour Holter recordings were performed. In addition, electrocardiogram, blood pressure, and plasma concentration of barucainide were measured. In 9 of 12 patients dose titration was effective (mean dose, 185 mg). In six of nine patients arrhythmia suppression persisted during maintenance therapy (mean dose, 18 mg/hr). Plasma concentrations correlated with given doses, rather than with antiarrhythmic efficacy. During the washout period, five patients required more than 12 hours for recurrence of arrhythmias. Treatment was stopped in one patient because of proarrhythmia; one patient had moderate heat sensations. Thus barucainide is a potent class IB agent, with a favorable side effect profile.

Anti-Arrhythmia Agents↗

PubMed1991

Endogenous atrial natriuretic factor is involved in the natriuresis following sodium loading in rats with chronic heart failure.

STUDY OBJECTIVE: Plasma levels of atrial natriuretic factor are increased in chronic heart failure; however, it is still controversial whether these raised levels contribute to the diuresis and natriuresis in this setting. To address this issue the potential contribution of endogenous atrial natriuretic factor in the renal excretion of a moderate oral sodium load in a rat model of chronic heart failure was studied. DESIGN: A monoclonal antibody against atrial natriuretic factor was used for specific antagonisation of its in vivo effects. Animals were subjected to oral sodium loading (30 ml.kg-1 0.9% NaCl, 2.5% dextrose) at baseline, immediately after, and 5 d after injection of monoclonal antibody or control solvent. EXPERIMENTAL MATERIAL: Sham operated rats and rats with chronic heart failure due to myocardial infarction (infarct size 35(SEM 4)% of left ventricle) were studied 4-5 weeks after surgery. MEASUREMENTS AND MAIN RESULTS: The renal excretion of cyclic guanosine monophosphate (cGMP), which represents a specific marker for the activation of the atrial natriuretic factor system, was markedly increased in infarcted rats, at 17.9(SEM 3.4) vs 5.8(1.2) nmol.kg-1, p less than 0.01. Atrial natriuretic factor antibody given immediately before sodium loading reduced the natriuretic response (0-4 h period) in infarcted rats from 1270(171) to 805(76) mumol.kg-1 (p less than 0.01) but not in sham operated animals. Similarly, the excretion of cGMP was only decreased by atrial natriuretic factor antibody in infarcted rats, from 29.8(6.3) to 20.7(3.7) nmol.kg-1. The reduction in sodium and cGMP excretion in infarcted rats was confirmed with a purified antibody preparation. CONCLUSIONS: Endogenous atrial natriuretic factor appears to be involved in the natriuresis following a moderate oral volume load in chronic heart failure. Thus the raised concentrations found in chronic heart failure may contribute to the regulation of urinary sodium excretion under these conditions despite the fact that the diuretic effects of exogenous atrial natriuretic factor are attenuated in chronic heart failure.

Animals↗

PubMed1991

The heart in heart failure. Ventricular and myocardial alterations.

In heart failure, many alterations occur in the ventricle as a whole, as well as in the myocardial cell. In the first part of this review we report on the macroscopic structure of the left ventricle by analysing the relation between left ventricular dilatation and left ventricular hypertrophy in terms of ventricular wall stress. Peak systolic stress in dilated ventricles of patients with compensated heart failure does not differ from values obtained in normal ventricles, whereas the systolic stress-time integral is increased by more than 40%. The stress-time integral is a major determinant of myocardial oxygen consumption, and its reduction by peripheral vasodilation leads to a proportional decrease in left ventricular oxygen consumption. In contrast, the phosphodiesterase inhibitor, enoximone, decreases the stress-time integral without a proportional decrease in myocardial oxygen consumption, due to the competition between positive inotropic effect with increased oxygen consumption and a vasodilating effect with decreased oxygen consumption. Beta-1 adrenoceptor agonists increase myocardial oxygen consumption. In the second part of this review we report on the functional alterations of the following subcellular and molecular structures in the failing myocardium: (1) adrenoceptors and G-proteins; (2) sarcoplasmic reticulum with an altered force-frequency relationship; (3) the acto-myosin system with decreased velocity of shortening and increased economy of force generation. On the basis of these alterations, a disadvantageous chain of events develops in the failing myocardial cell.

Cardiomegaly↗

PubMed1991

The effect of the partial beta-1-adrenoceptor agonist xamoterol on hemodynamics and myocardial energetics in patients with idiopathic dilated cardiomyopathy.

Xamoterol, a new partial beta 1-adrenoceptor agonist, was evaluated in respect to its hemodynamic and energetic effects when given acutely i.v. (0.2 mg/kg body weight) to 10 patients with idiopathic dilated cardiomyopathy. Hemodynamically, a small drop in left ventricular end-systolic volume index (from 105 +/- 38 to 91 +/- 48 ml/m2; p less than 0.05) and end-diastolic volume index (from 168 +/- 44 to 152 +/- 41 ml/m2; p less than 0.05) and an increase in maximum rate of left ventricular pressure rise (from 1,003 +/- 358 to 1,283 +/- 398 mm Hg/s; p less than 0.001) was observed. The systolic stress-time integral was only slightly reduced after injection of xamoterol, from 107 +/- 28 to 94 +/- 35 x 10(3) dyn.s/cm2 (NS). Other conventional hemodynamic variables did not change significantly. Myocardial oxygen consumption per beat increased from 125 +/- 39 microliters/beat/100 g to 153 +/- 62 microliters/beat/100 g (p less than 0.05). The ratio of myocardial oxygen consumption per beat and stress-time integral--as an inverse measure of left ventricular contraction economy--increased significantly, from 132 +/- 62 to 192 +/- 115 microliters/beat/10(3) dyn.s/cm2 (p less than 0.02) after injection of xamoterol, whereas left ventricular efficiency decreased from 17.6 +/- 7.8 to 13.8 +/- 6.5% (p less than 0.05). Thus, in idiopathic dilated cardiomyopathy, xamoterol exhibited only minor hemodynamic effects whereas myocardial contraction economy and efficiency were significantly reduced.

Adult↗

PubMed1991

Mechanisms involved in the response to prolonged infusion of atrial natriuretic factor in patients with chronic heart failure.

We examined the mechanisms involved in the cardiovascular and renal response to prolonged infusion of atrial natriuretic factor (ANF) in patients with chronic heart failure. ANF infusion was titrated to produce a 30% decrease in pulmonary capillary wedge pressure or a 20% increase in cardiac output, and this dose (average, 75 +/- 4 ng/kg/min) was then administered for 20 hours. The short-term response to ANF included significant reductions in central filling pressures, increases in cardiac output, modest increases in diuresis and glomerular filtration rates, significant reduction in plasma aldosterone levels, and a 3.6-fold increase in plasma cyclic GMP levels. During prolonged infusion, plasma cGMP levels and cardiac output gradually returned to baseline. Similarly, the initially increased diuretic effects were completely abolished during prolonged ANF infusion, although plasma alpha-hANF levels remained consistently elevated above baseline values (control, 198 +/- 38; titration, 2,760 +/- 596; 20 hours, 3,499 +/- 659 pg/ml). Four hours after beginning the ANF infusion, marked increases in hematocrit levels were noted (42.5 +/- 1.0% versus 45.3 +/- 1.4%, control and infusion, respectively, p less than 0.05); during this time, no change in total plasma protein concentration occurred, indicating extravascular shift of fluid and plasma proteins. No evidence was noted for activation of vasoconstrictor hormones during prolonged ANF infusion, although mean arterial pressure was significantly reduced throughout the infusion period. Plasma pro-ANF (31-67) levels, determined as a marker for endogenous ANF secretion, were significantly suppressed as were the reductions of central filling pressures. After ANF discontinuation, heart rate and pulmonary capillary wedge pressure increased significantly above baseline values without evidence for sympathetic stimulation. We conclude that 1) prolonged infusion of ANF causes only transient increases in plasma cGMP levels but a sustained reduction of the cardiac release of ANF and that 2) the beneficial hemodynamic effects of ANF, that is, unloading of the ventricles, may be associated with or, in part, may be secondary to a shift of plasma constituents into the extravascular space. The latter may limit the therapeutic potential of ANF for long-term treatment.

Atrial Natriuretic Factor↗

PubMed1991

Modulation of coronary vasomotor tone in humans. Progressive endothelial dysfunction with different early stages of coronary atherosclerosis.

The endothelium plays a critical role in the control of vasomotor tone by the release of vasoactive substances. Because endothelial injury or dysfunction is considered important very early in atherogenesis, we hypothesized that abnormal endothelial function precedes the angiographic detection of coronary atherosclerosis in the human coronary circulation. The coronary vasomotor responses to three different endothelium-mediated stimuli (intracoronary infusion of acetylcholine 10(-8) to 10(-6) M, increase in blood flow to induce flow-dependent dilation, and sympathetic stimulation by cold pressor testing) were assessed by quantitative angiography and subselective intracoronary Doppler flow velocity measurements within the left anterior descending coronary artery in 38 patients. All three stimuli elicited epicardial artery dilation in all 11 patients with smooth coronary arteries and absence of risk factors for coronary artery disease (group 1). All nine patients with smooth coronary arteries but with hypercholesterolemia (group 2) demonstrated a selective impairment in endothelial function with vasoconstriction (35 +/- 12.7% decrease in mean luminal area) in response to acetylcholine but showed a preserved flow-dependent dilation (15.5 +/- 4.4% increase in mean luminal area) and vasodilation in response to cold pressor testing (14.2 +/- 4.6% increase in mean luminal area). In all nine patients with an angiographically defined smooth coronary artery segment but with evidence of atherosclerosis elsewhere in the coronary system (group 3), both acetylcholine and cold pressor testing induced vasoconstriction (26.2 +/- 8.7% and 18.7 +/- 7.9% decrease in mean luminal area, respectively), whereas flow-dependent dilation was preserved (20.4 +/- 8.7% increase in mean luminal area). In the nine patients with angiographic evidence of wall irregularities (group 4), flow-dependent dilation was also abolished and vasoconstriction occurred in response to acetylcholine and cold pressor testing (34.5 +/- 10.7% and 19.9 +/- 6.3% decrease in mean luminal area, respectively). All coronary artery segments dilated in response to nitroglycerin, suggesting preserved function of vascular smooth muscle. Despite similar reductions in coronary vascular resistance in response to the smooth muscle relaxant papaverin, patients with hypercholesterolemia demonstrated a selective impairment of vasodilation of the resistance vasculature in response to acetylcholine (p less than 0.05 versus groups 1, 3, and 4). Thus, there is a progressive impairment of endothelial vasoactive functioning in coronary arteries of patients with different early stages of atherosclerosis, beginning with a selective endothelial dysfunction in angiographically defined normal arteries in patients with hypercholesterolemia and progressively worsening to a complete loss of endothelium-mediated vasodilation in angiographically defined atherosclerotic coronary arteries.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗

PubMed1991

Intracoronary thrombus formation causes focal vasoconstriction of epicardial arteries in patients with coronary artery disease.

BACKGROUND: Experimental studies have demonstrated that intracoronary platelet aggregation and thrombus formation may induce marked vasoconstriction of epicardial arteries with endothelial injury. METHODS AND RESULTS: To examine the effects of intracoronary thrombus formation on coronary vasomotor tone of human epicardial arteries in vivo, we studied 15 patients who developed intracoronary thrombi adherent to the guide wire during balloon dilatation. Epicardial artery luminal area was evaluated by quantitative coronary angiography proximal and distal to the site of intracoronary thrombus formation and in a reference vessel before and after thrombus formation as well as after intracoronary injection of 0.2-0.3 mg nitroglycerin. All artery segments distal to the site of thrombus formation showed vasoconstriction with a luminal area reduction of -27.4 +/- 17.1% (p less than 0.001), whereas proximal vessel segments and reference vessels not manipulated during percutaneous transluminal coronary angioplasty did not demonstrate any significant luminal area changes during thrombus formation. Angiographic measurements after advancing the guide wire with the adherent thrombus (performed in six of the 15 patients) revealed in all patients that vasoconstriction did develop at a new site distal to the thrombus persistence of the initial vasoconstriction now residing proximal to the thrombus. Thus, there was a sequential association between thrombus formation and subsequent distal vasoconstriction. Intracoronary injection of nitroglycerin abolished the thrombus-induced vasoconstriction. No significant luminal area changes were observed in 20 patients without angiographic evidence of intracoronary thrombus formation. CONCLUSIONS: Intracoronary thrombus formation during percutaneous transluminal coronary angioplasty causes focal vasoconstriction of epicardial arteries in patients with coronary artery disease. Although caution must be advised in the extrapolation of this phenomenon, which was observed in a manipulated artery during coronary angioplasty, the vasoconstrictor response to intracoronary thrombus formation in vivo may play an important role in the dynamic mechanisms of acute coronary heart disease syndromes.

Angiography↗

PubMed1991

Endothelial dysfunction of the coronary microvasculature is associated with coronary blood flow regulation in patients with early atherosclerosis.

BACKGROUND: The vascular endothelium is capable of regulating tissue perfusion by the release of endothelium-derived relaxing factor to modulate vasomotor tone of the resistance vasculature. METHODS AND RESULTS: To test whether atherosclerosis is associated with a functional abnormality of endothelium-mediated microvascular relaxation affecting coronary blood flow regulation, we compared coronary blood flow responses with cold pressor testing with the response of the coronary vasculature to acetylcholine (an endothelium-dependent vasodilator) and to papaverin (a direct dilator of vascular smooth muscle) in 12 normal control patients and in 19 patients with non-flow-limiting epicardial atherosclerosis (CAD). The drugs were subselectively infused into the left anterior descending coronary artery via a Doppler catheter, and the response in coronary blood flow was assessed by measuring intracoronary blood flow velocity and cross-sectional arterial area (quantitative angiography). Coronary vascular resistance decreased in all normal control patients by -24.1 +/- 5.5% (mean +/- SD) during the cold pressor test, whereas the CAD patients demonstrated a variable coronary vascular resistance response to cold pressor testing despite comparable changes in the rate-pressure product. The slopes of the acetylcholine dose-blood flow response (percent change in coronary blood flow/dosage of acetylcholine) were significantly reduced in the CAD patients with 38.5 +/- 24.8 compared with the normal patients (80.8 +/- 28.1; p less than 0.001). Although coronary blood flow responses to papaverin were slightly but significantly (p less than 0.05) reduced in the CAD patients, the response to the endothelium-dependent dilator acetylcholine was considerably out of proportion to the papaverin response in these patients compared with the normal patients. The capacity of the coronary system to increase blood flow in response to acetylcholine expressed as relative proportion of the maximal papaverin response was 52.5 +/- 18.2% in the normal control patients but only 33.6 +/- 23.6% in the CAD patients (p less than 0.025 versus normals). There was a significant negative correlation (r = -0.69; p less than 0.0001) between cold pressor test-induced changes in coronary vascular resistance and the capacity of the coronary system to increase blood flow in response to acetylcholine. CONCLUSIONS: Early stages of epicardial atherosclerosis are associated with an impairment in endothelium-dependent dilation of the coronary microvasculature, indicating that the pathophysiological consequences of atherosclerosis may extend into the human coronary microcirculation. The correlation between cold pressor test-induced coronary vascular resistance changes and the extent of endothelial dysfunction suggests a relation between endothelial function of the microvasculature and coronary blood flow regulation during sympathetic stimulation associated with increased myocardial work.

Acetylcholine↗

PubMed1991

Cilazapril in congestive heart failure. A pilot study.

The haemodynamic effects of a single dose of cilazapril 2.5 or 5 mg were studied in 33 patients with stable chronic congestive heart failure who were receiving digitalis and diuretics. Subsequently, a double-blind comparison of the haemodynamic and clinical effects of 3 months' treatment with cilazapril 1.25 to 5 mg daily or placebo in 24 evaluable patients revealed that the acute haemodynamic improvement produced by a single dose of cilazapril was maintained in patients receiving repeated administration of the drug, but not in those randomly allocated the placebo. Acute cilazapril significantly decreased mean arterial pressure, systemic vascular resistance, pulmonary capillary wedge pressure, pulmonary artery pressure and right atrial pressure, while cardiac index and stroke volume index increased at rest and during submaximal exercise. After 3 months' treatment 11 of 13 cilazapril recipients improved their New York Heart Association (NYHA) class compared with 2 of 11 patients treated with placebo. This functional improvement was paralleled by a patient-perceived improvement in general well-being.

Adult↗

PubMed1991

Left ventricular geometry, myocardial function and energetics of the dilated left ventricle. Influence of vasodilators and positive inotropic substances.

Vasodilators have been shown to improve hemodynamics of the failing heart as a short-term effect and to decrease mortality as a long-term result. We therefore studied the effect of different vasodilators on myocardial mechanics and energetics in patients with idiopathic dilated cardiomyopathy (IDC) NYHA II to III. In these patients undergoing routine heart catheterization myocardial oxygen consumption was measured using the argon method, and left ventricular pressure and geometry were obtained from left ventricular angiography using a Millar tip microcatheter. All data were analyzed for one single heart beat. The best correlation was found between MVO2/beat and the systolic stress-time integral which considers left ventricular pressure, wall thickness, and geometry. The relation between MVO2/beat and peak systolic wall stress was less relevant. No correlation was found between MVO2/beat and pressure-volume work, dP/dtmax, and mean velocity of circumferential fiber shortening. The intravenous application of nitroprusside and the ACE-inhibitor benazepril decreased both the systolic stress-time integral and the myocardial oxygen consumption in proportion to each other indicating unchanged economy of myocardial contraction. In contrast to other vasodilators, beta 1-agonists and phosphodiesterase inhibitors increase myocardial oxygen consumption independently of changes in the stress-time integral. In conclusion, vasodilators decrease left ventricular pressure and chamber size and thereby proportionally reduce MVO2/beat. The reduction of energy needed for myocardial contraction may partially explain the long-term effects of the ACE-inhibitors and combinations of vasodilators. Pure positive inotropic substances, especially beta 1-agonists, increase myocardial oxygen consumption with minor changes of systolic stress-time integral.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Volume↗

PubMed1991

[Arrhythmia and anti-arrhythmia therapy as prognostic risks].

The incidence of sudden death is estimated to be 0.25%/year in the industrialized world. 30 to 40% of patients are known to be at major risk before they succumb sudden death. Etiology is usually coronary heart disease (75%), dilated and hypertensive cardiomyopathy as well as valvular disease. 75% of patients dying suddenly die from ventricular fibrillation. The most common mechanism of sudden cardiac death in heart failure is sustained ventricular tachycardia deteriorating into ventricular fibrillation, the initiating factors being single ventricular beats, ventricular pairs or nonsustained ventricular tachycardia (trigger mechanism). At least 50% of patients dying during Holter monitoring have been on antiarrhythmic treatment during the time of sudden death and this percentage is increased to 70% in patients dying from torsade de pointes ventricular tachycardia. The question that has arisen is whether suppression of such arrhythmias by antiarrhythmic agents will reduce the incidence of sudden cardiac death. Unfortunately, the patient group at highest risk - low ventricular ejection fraction and high incidence of nonsustained ventricular tachycardia episodes during 24 hour-monitoring and thus, the group most in need of arrhythmia suppression - has the lowest responder rate as well as the highest incidence of serious toxicity. Until the suppression of those arrhythmias by antiarrhythmic agents is demonstrated to improve prognosis in this patient group, routine use of antiarrhythmic agents cannot be recommended in this patient population.

Anti-Arrhythmia Agents↗

PubMed1991

Energetic consequences of substances currently used or recommended for long-term treatment of chronic heart failure.

Vasodilators have been shown to improve hemodynamics of the failing heart as a short-term effect, and to decrease mortality as a long-term result. We, therefore, studied the effects of vasodilators and inotropic agents on myocardial mechanics and energetics in patients with congestive heart failure New York Heart Association (NYHA) classes II-III. In these patients, who underwent routine heart catheterization, myocardial oxygen consumption was measured using the argon method, and LV pressure and geometry were obtained from LV angiography using a Millar microtipped catheter. All data were analyzed for one single heart beat. The best correlation was found between MVO2/beat and the systolic stress-time integral which considers LV pressure, LV wall thickness, and LV geometry. The relation between MVO2/beat and peak systolic wall stress was less relevant. No correlation was found between MVO2/beat and pressure-volume work, dP/dtmax, and mean velocity of circumferential fiber shortening. The intravenous application of nitroprusside and the ACE-inhibitor benazepril decreased both the systolic stress-time integral and the myocardial oxygen consumption in proportion to each other, indicating unchanged economy of myocardial contraction. In contrast, beta 1-agonists and phosphodiesterase inhibitors increased myocardial oxygen consumption independently of changes in the stress-time integral. In conclusion, vasodilators decrease LV pressure and chamber size and thereby proportionally reduce MVO2/beat. The reduction of energy needed for myocardial contraction may partially explain the long-term effects of the ACE-inhibitors and combinations of vasodilators. Pure inotropic substances, especially beta 1-agonists, increase myocardial oxygen consumption with only minor changes of systolic stress-time integral.(ABSTRACT TRUNCATED AT 250 WORDS)

Benzazepines↗

PubMed1991

[Vasodilatation and positive inotropic effect of the phosphodiesterase inhibitor enoximone].

The comparison of two invasive studies using intravenous application of the phosphodiesterase enoximone demonstrated unchanged cardiac output in patients with dilated cardiomyopathy NYHA II-III, and increased cardiac output (from 3.22 +/- 1.15 to 5.04 +/- 2.05 l/min; p less than 0.01) in acute heart failure. This comparison of hemodynamic parameters in addition to studies on myocardial oxygen consumption support the use of intravenous enoximone in acute heart failure, whereas the long-term application of enoximone in chronic heart failure is judged to be critical.

Cardiac Output↗