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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Central haemodynamics and regional blood flow were studied comprehensively in conscious New Zealand White rabbits before and during the development of chronic low output cardiac failure produced by administration of the anticancer agent adriamycin. After eight weeks of adriamycin treatment, cardiac index fell from 326(40 to 225(56) ml.min-1.kg-1. This was accompanied by an increase in heart rate and total peripheral resistance but no change in mean systemic blood pressure. Myocardial function was shown to be depressed by the measurement of Frank-Starling curves, the slopes of which were appreciably flatter in adriamycin treated rabbits. Regional blood flow (measured by the radioactive microsphere technique) was redistributed. There were decreases in renal, splenic, small gut, and skeletal muscle blood flow, whereas myocardial and cerebral blood flow were unchanged. There was an increase in total body exchangeable sodium, indicating some salt and water retention. Systemic toxic effects of adriamycin could be limited by treating the animals for eight weeks with adriamycin and then allowing a two week recovery period before haemodynamic study. This would appear to be the optimal dosage schedule.
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PMID:An experimental model of chronic cardiac failure using adriamycin in the rabbit: central haemodynamics and regional blood flow. 366 39

Exercise investigations were performed in 39 male hypertensives (WHO stage I-III) to assess haemodynamics and cardiac function after intravenous application of 5 mg propranolol for the detection of latent heart failure. Radiocardiography was used to determine volumetric parameters such as LV end-diastolic volume and ejection fraction, and microcatheterization was employed to obtain the LV filling pressure via pressure measurement in the pulmonary artery (PA). The negative inotropic and chronotropic effects of propranolol on pump function and myocardial mechanics at rest were found to be minimal. During 50 watt exercise however, an increase of the diastolic PA pressure has been observed simultaneously with a diminution of cardiac output (stroke volume being constant). Thus, under acutely administered beta blockade, a general disturbance in the flow-pressure relation could be induced, being comparable to heart failure. Only in a few cases was the reduced contractility compensated by the Frank-Starling mechanism, but only if the mechanism did not participate in the regulation of pump function during the previous control investigation. In other cases a remarkable reduction of cardiac output and even stroke volume occurred, results which may be explained as a consequence of a reduced venous return (or pooling) connected with acutely induced vascular effects (beta-2 blockade).
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PMID:[Differing acute effects of propranolol on the hypertensive heart during exercise]. 377 88

The acute hemodynamic response to a single oral dose of nitrendipine (10-20 mg) was evaluated in eight subjects with severe chronic congestive heart failure during right heart catheterization. A hemodynamic effect began within 1 h. At peak effect (1-2 h after drug administration), mean arterial pressure fell from 84.0 +/- 9.2 to 76.0 +/- 9.2 mm Hg (mean +/- SD), right arterial pressure from 10.6 +/- 5.9 to 8.0 +/- 7.1 mm Hg, mean pulmonary arterial pressure from 35.5 +/- 9.2 to 30.1 +/- 9.4 mm Hg, pulmonary wedge pressure from 23.6 +/- 6.7 to 17.7 +/- 6.3 mm Hg, and cardiac index rose from 1.91 +/- 0.38 to 2.45 +/- 0.34 L/min/m2. Heart rate did not change (85 +/- 18 to 82 +/- 18 beats/min) despite the significant fall in arterial pressure. Systemic and pulmonary vascular resistances fell significantly. Whereas forearm blood flow increased from 1.44 +/- 0.52 to 2.06 +/- 0.41 ml/min/100 g (p less than 0.05), hepatic and renal blood flows were unchanged. This study demonstrates the acute effectiveness of nitrendipine in reducing ventricular preload and impedance in heart failure and in increasing cardiac output that appears to be preferentially directed to the skeletal bed. The left-upward shift of the Frank-Starling curve suggests the absence of any clinically important negative inotropic effect of nitrendipine. Nitrendipine therefore may be a useful agent for vasodilator therapy of heart failure.
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PMID:Acute hemodynamic effects of nitrendipine in chronic congestive heart failure. 608 56

We report the management of a patient with chronic idiopathic thrombocytopenic purpura and mitral valve disease. Although a two-stage approach was planned (splenectomy followed by mitral valve replacement one month later), the patient developed medically-resistant heart failure, and splenectomy plus mitral valve replacement were performed during the same operation. The platelet count at operation was 20,000/mm3. Platelet transfusion, used at the end of cardiopulmonary bypass, was considered no longer necessary in the postoperative period, as the platelet count quickly increased after the first postoperative day. The postoperative course was uneventful. Though we believe the two-stage surgical approach is preferable, our case shows that open-heart operations and splenectomy can be successfully performed simultaneously in patients with idiopathic thrombocytopenic purpura.
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PMID:Mitral valve replacement and splenectomy in a patient with chronic idiopathic thrombocytopenic purpura. 618 2

There is evidence that sarcomere length is maximal and changes little during chronic cardiac enlargement, and that the failing heart does not operate on a true descending limb of the Frank-Starling curve. However, increases of ventricular end-diastolic volume over time clearly are important at the geometrical level in maintaining stroke volume. When the preload reserve is fully utilized, afterload mismatch can exist in the steady state to produce operation of the heart on an apparent descending limb of cardiac function, and further afterload mismatch can be produced by pressure loading under these conditions. The treatment of acute experimental heart failure with a mixed vasodilator (nitroprusside) can lead to an increased cardiac output by afterload reduction only when the venous return curve does not shift downward; thus, the threefold larger shift of central blood volume to the periphery in heart failure (compared to normal) counter balances the venodilator action of nitroprusside. Whether or not the inotropic ceiling of failing myocardium can be reached by positive inotropic agents is unclear, but major hemodynamic benefits in heart failure with many potent inotropic drugs are associated with the direct vasodilating properties of these agents. Thus, there appears to be little role for the Frank-Starling mechanism at the sarcomere level, whereas afterload mismatch and its correction are of major importance provided the venous return can be increased. A degree of inotropic reserve also is available, even in the severely failing myocardium, but more research is needed on the potential costs and benefits of marked sustained inotropic stimulation.
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PMID:Mechanisms of cardiac contraction. What roles for preload, afterload and inotropic state in heart failure? 622 Aug 96

Nitroglycerin, when administered to patients with heart failure, causes a marked reduction in left ventricular filling pressure but often an increase in stroke volume and stroke work; based on the Frank-Starling principle, such a reduction in "preload" would be expected to result in a decrease in left ventricular end-diastolic volume and, therefore, a decline in stroke volume. Assessment of pressure-volume coordinates, however, has revealed that nitroglycerin produces a downward shift in the pressure-volume relationship. This apparent improvement in left ventricular compliance cannot be attributed to alterations in the elastic properties of the myocardium but rather appear to reflect a reduction in left ventricular external constraint. Recent animal and clinical investigations in our laboratory suggest that nitroglycerin causes venous dilatation (particularly in the mesenteric bed), thereby decreasing venous pressure at any given vascular volume. This decrease in cardiac filling pressure results in a decrease in heart size and, therefore, a reduction in pericardial pressure. Left ventricular transmural (intracavitary minus pericardial) pressure is little changed, however, so that end-diastolic volume and stroke volume are maintained.
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PMID:Mechanism of action of nitrates. Role of changes in venous capacitance and in the left ventricular diastolic pressure-volume relation. 643 73

Forty-two patients aged 35 to 58 years with arterial hypertension were examined. The patients did not manifest any clinical signs of heart failure or coronary heart disease. All the patients were subjected to the leg form of isometric exercise test with a 100% maximal force. The blood pressure, heart rate, heart contractility and pump function were examined in the course of the test. It was demonstrated that in patients with arterial hypertension, the pressor reactions in response to the exercise were similar to those in healthy subjects but were more pronounced. In patients with stage IIA arterial hypertension, the increase of blood pressure occurred due to the inotropic reaction of the myocardium and triggering of Frank-Starling's mechanism. In patients with stage IIB arterial hypertension, the increase of blood pressure was caused by the total peripheral resistance elevation. The leg form of isometric exercise permits the detection of early signs of heart failure in patients with arterial hypertension.
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PMID:[Hemodynamic changes in patients with arterial hypertension during isometric exercise]. 649 11

Different types of heart rate (HR)-cardiac output (COP) relationships were compared with their clinical features and hemodynamic findings in 56 patients with brady-arrhythmias (BA). HR was raised by increments of 10 beats per minute (bpm) at 3 min intervals, from spontaneous rates to 100 or 110 bpm by right ventricular pacing. Cardiac and left ventricular (LV) functions at BA were evaluated by intra-cardiac pressures, COP measured by the thermo-dilution method and echocardiographic data. HR-COP relationships were divided into the following 3 types: 24 patients of flat (F), 18 of peaked (P) and 14 of increased (I) type. There were more patients with complete atrio-ventricular block, particularly His-ventricular block, and cardiomyopathic patients with the "P" type than with the other types. Cardiac index, stroke index, stroke work index and systemic vascular resistance were greater in "I", but these differences were not significant. LV peak systolic pressure (LVSP) and end-diastolic pressure (EDP) in "I" increased more than in "F". EDP, LV end-diastolic and end-systolic dimension (ESD) in "P" increased more than in "F". Systolic excursion and LVSP/ESD ratio in "I" increased more than in the other types. Heart failure prior to implantation of pacemaker (PM) and post-PM occurred more frequently in "P". "F" and "I" patients showed comparatively good clinical courses after PM. Thus, cardiac and LV function during BA are maintained in "F" and are impaired in "P", as reported previously. On the other hand, cardiac functions are maintained in "I" as they are in "F", mainly due to contributions of the Frank-Starling mechanism and partly due to maintenance or slight augmentation of contractility.
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PMID:Reconsideration of heart rate-cardiac output relationships and resting cardiac function in patients with brady-arrhythmias. 651 89

We investigated ventricular interaction by the use of six excised, perfused, canine hearts. In this preparation, we could change the filling pressure of the right and left ventricles independently, thereby breaking the normal series-pump arrangement. We found that mechanical ventricular interaction exists in diastole and in systole. Namely, not only decreased diastolic ventricular compliance, but also the reduced performance in either ventricle was found, when the opposite ventricular pressure was increased. Thus, when the opposite ventricular filling pressure increases, we suspect that systolic ventricular function of either ventricle will be depressed significantly by these two factors; i.e., the Frank-Starling effect due to decreased ventricular diastolic volume following decreased diastolic ventricular compliance, and the depressed systolic ventricular function. Clinically, these findings may be important in considering the mechanism of the occurrence of simultaneous reduced performance of both ventricles in cases when only one side of the ventricle is affected hemodynamically and its filling pressure is greatly increased in various pathological states such as heart failure.
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PMID:Mechanical interaction between the ventricles. 665 41

We evaluated the effects of intravenous verapamil, a calcium antagonist, on hemodynamics and regional left ventricular (LV) performance in patients with acute myocardial infarction (AMI). Twenty patients having uncomplicated infarction or moderate heart failure were randomized to receive either verapamil or placebo and were studied a mean of 12 hours after onset of symptoms. Verapamil, 7.5 mg intravenously, acutely reduced systolic arterial pressure (p less than 0.0005), systemic vascular resistance, and LV stroke work (p less than 0.005) and rate-pressure product (p less than 0.05); the heart rate did not alter. The Frank-Starling relationship by Swan-Ganz catheter did not change for 1 hour. Segmental wall motion amplitudes were recorded from eight standardized segments around the left ventricle by a multidirectional M-mode echocardiographic technique. The systolic wall motion of the uninvolved LV segments and LV cavity size did not change after verapamil. Verapamil improved mechanical performance in the ischemic segments (p less than 0.005). Therefore, the overall regional contractile function of the left ventricle improved as well (by 11% to 13%, p less than 0.05). This echocardiographic improvement continued after the acute vasodilatory response of intravenous verapamil subsided and was preserved for 1 week, the patients having had oral verapamil, 240 mg daily. Chest pain was relieved in five of the six patients having ongoing slight pain before verapamil injection. No sequential hemodynamic or echocardiographic changes occurred in the placebo-treated patients. Thus, in patients with uncomplicated AMI, verapamil improve contractile function of the acutely ischemic LV segments by hemodynamic unloading and/or by direct myocardial effect, without manifest depression of the uninvolved myocardium.
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PMID:Effects of verapamil in patients with acute myocardial infarction: hemodynamics and function of normal and ischemic left ventricular myocardium. 669 58


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