Effects of ouabain on myocardial oxygen supply and demand in patients with chronic coronary artery disease. A hemodynamic, volumetric, and metabolic study in patients without heart failure.

The effects of digitalis glycosides on myocardial oxygen supply and demand are of particular interest in the presence of obstructive coronary artery disease, but have not been measured previously in man. We assessed the effects of ouabain (0.015 mg/kg body weight) on hemodynamic, volumetric, and metabolic parameters in 11 patients with severe chronic coronary artery disease without clinical congestive heart failure. Because the protocol was long and involved interventions which might affect the determinations, we also studied in nine patients using an identical protocol except that ouabain administration was omitted. Left ventricular end-diastolic pressure and left ventricular end-diastolic volume fell in each patient given ouabain, even though they were initially elevated in only two patients. Left ventricular end-diastolic pressure fell from 11.5+/-1.4 (mean+/-SE) to 5.6+/-0.9 mm Hg (P less than 0.001) and left ventricular end-diastolic volume fell from 100+/-17 to 82+/-12 ml/m2 (P less than 0.01) 1 h after ouabain infusion was completed. The maximum velocity of contractile element shortening increased from 1.68+/-0.11 ml/s to 2.18+/-0.21 muscle-lengths/s (P less than 0.05) and is consistent with an increase in contractility. No significant change in these parameters occurred in the control patients. No significant change in myocardial oxygen consumption occurred after ouabain administration but this may be related to a greater decrease in mean arterial pressure in the ouabain patients than in the control patients. We conclude that in patients with chronic coronary artery disease who are not in clinical congestive heart failure left ventricular end-diastolic volume falls after ouabain administration even when it is initially normal. Though this fall would be associated with a decrease in wall tension, and, therefore, of myocardial oxygen consumption, it may not be of sufficient magnitude to prevent a net increase in myocardial oxygen consumption. Nevertheless, compensatory mechanisms prevent a deterioration of resting myocardial metabolism.

Therapeutic defibrination and heparin therapy in the prevention and resolution of experimental venous thrombosis.

The application of phenol to the femoral veins of anesthetized dogs resulted in an occluding thrombus in 24 of 25 veins at 1 week. Serial venography and eventual histology showed that these veins remained occluded over a 5-week observation period, the thrombi undergoing organization. Therapeutic defibrination was achieved with administration of an enzyme from venom of the pit viper (Arvin). Arvin, administered for 1 week immediately following phenol application and before thrombus formation had occurred, prevented thrombosis in all 10 such veins, and serial venography for a further 4 weeks showed that the veins remained patent. Administration of Arvin was begun 24 hours postoperatively, when venography had demonstrated an occluding thrombus and failed to clear any of 11 veins after 3 weeks of treatment. Intravenous administration of heparin, 10,000 units, at 6, 6, and 12-hour intervals in a 24-hour period, was begun immediately after phenol application and continued for 1 week; 10 of 12 veins were blocked at 1 week. Following the same dose of heparin every 6 hours four of eight veins were blocked at 1 week. The results indicate that when the vascular endothelium is damaged, therapeutic defibrination is more effective than heparin therapy in preventing venous thrombosis. Arvin therapy has no significant thrombolytic effect even if the thrombus is less than 24 hours old.

Valvular heart disease: a perspective.

Valve replacement has been one of the most important advances in the management of patients with valvular heart disease. The 10 and 15 year survival rate after isolated aortic and mitral valve replacement with the Starr-Edwards valve is 56 and 44%, respectively. At 5 and 7 years, survival with the Björk-Shiley, porcine bioprosthesis and the Starr-Edwards valve is similar. Patients operated on during the last 5 to 10 years have a much better survival rate than those operated on in the 1960s; therefore, the 10 and 15 year survival of those operated on recently should improve. All patients with a mechanical prosthesis need long-term anticoagulant therapy with drugs of the coumadin type. Porcine bioprostheses have a low failure rate up to 5 years after valve replacement; after this, valve failure occurs at an increasing rate, but the incidence at 10 and 15 years is not known. Valve replacement usually produces a marked improvement in the symptomatic status of the patient because of improved hemodynamics; ventricular function is improved in selected subsets of patients. The role of long-term vasodilator therapy has not been fully determined. Antibiotic prophylaxis for secondary prevention of rheumatic carditis and for prevention of infective endocarditis is important.

Survival 15 to 20 years after coronary bypass surgery for angina.

OBJECTIVES: The aim of this study was to determine the 15- to 20-year outcome of coronary bypass surgery in patients with angina. BACKGROUND: Coronary bypass surgery has been performed for > 20 years; we need to know the expected outcome of a very long-term follow-up. METHODS: Using actuarial techniques, we determined the outcome of coronary bypass surgery performed for chronic stable and unstable angina in 7,529 patients from 1969 to 1988. RESULTS: The 5-, 10-, 15- and 20-year survival rates (mean +/- SE) were 88 +/- 1, 73 +/- 1, 53 +/- 1 and 38 +/- 3%, respectively, for the whole group. Compared with patients operated on in 1974 to 1988 (n = 7,026), patients operated on in 1969 to 1973 (n = 503) were younger and had less coronary artery disease but had a higher operative mortality rate and a shorter long-term survival time; 15- and 20-year survival of the 1969 to 1973 cohort was 47 +/- 2% and 33 +/- 3%, respectively. The 1974 to 1988 cohort of patients had a 2.1% operative mortality rate and a 10- and 15-year survival probability of 74 +/- 1% and 55 +/- 2%, respectively. For 2,128 patients with "normal" left ventricular function, the 10- and 15-year survival probability was 82 +/- 1% and 64 +/- 3%, respectively, and for 2,413 patients with "abnormal" left ventricular function, it was 66 +/- 1% and 47 +/- 3%, respectively (p < 0.0001); for men it was 74 +/- 1% and 56 +/- 2%, respectively, and for women, 70 +/- 2% and 52 +/- 5%, respectively, p < 0.05. The actuarial percentages of reoperation and myocardial infarction at 15 years were 33 +/- 2% and 26 +/- 2%, respectively; these values did not differ significantly between men and women. There was a significant (p < 0.001) difference between men and women in angina status; 81% of the men versus 74% of the women had no angina or mild angina at the most recent follow-up study. CONCLUSIONS: Coronary bypass surgery is an effective form of therapy for angina (for 15 to 20 years) in both men and women.

Resistance to isosorbide dinitrate in patients with severe chronic heart failure: incidence and attempt at hemodynamic prediction.

Oral isosorbide dinitrate has been widely used to lower elevated left ventricular filling pressure in patients with chronic heart failure. Although the recommended dose of this drug is 40 mg every 6 h, failure to respond to this dose has been observed in many patients with heart failure. In the present study the incidence of resistance to isosorbide dinitrate was evaluated and an attempt was made to identify baseline hemodynamic predictors for this phenomenon in 50 patients with severe chronic heart failure due to left ventricular systolic dysfunction (mean left ventricular ejection fraction 0.23 +/- 0.08). Twenty-seven (54%) of the 50 patients responded to 40 mg of isosorbide dinitrate (greater than 20% decrease in mean pulmonary artery wedge pressure sustained greater than or equal to 1 h) and 23 patients (46%) failed to respond. Nonresponders to 40 mg of isosorbide dinitrate had a significantly higher baseline right atrial pressure than did responders (14 +/- 5 versus 10 +/- 6 mm Hg, p less than 0.02). In addition, all 7 patients with a baseline right atrial pressure of less than 7 mm Hg and 12 of 14 patients with a baseline right atrial pressure less than 10 mm Hg responded to 40 mg. No significant differences were noted between responders and nonresponders in any other baseline hemodynamic or clinical variables, or in peak isosorbide dinitrate serum levels (32 +/- 19 ng/ml in nonresponders versus 44 +/- 36 ng/ml in responders). Of the 23 nonresponders to 40 mg, 22 received a higher dose (80 to 120 mg).(ABSTRACT TRUNCATED AT 250 WORDS)

Response of angina and ischemia to long-term treatment in patients with chronic stable angina: a double-blind randomized individualized dosing trial of nifedipine, propranolol and their combination.

Seventy-four patients with chronic stable mild angina, mild coronary artery disease (83% had one- or two-vessel disease) and normal left ventricular function were studied to measure the response of treadmill exercise performance and painful and silent ischemia in the ambulatory setting to randomly assigned treatment with nifedipine or propranolol and their combination; titration to maximal tolerated dosages was performed in double-blind manner. At 3 months both nifedipine and propranolol reduced the weekly angina rate (p less than 0.05); during treadmill exercise testing, increases (p less than 0.05) were noted in time to angina and total exercise time and decreases in maximal ST depression at the end of exercise. There were no differences between the responses to nifedipine and propranolol and no significant additional changes were seen after another 3 months of therapy. The combination of nifedipine and propranolol reduced the number of patients with angina on exercise treadmill testing from 64% to 38% (p less than 0.05). During ambulatory electrocardiographic monitoring before treatment, there were 1.4 +/- 2.4 (mean +/- SD) episodes/24 h of painful ischemia and a very low silent ischemia frequency: mean 1.1 +/- 2.7 episodes/24 h, mean duration 16 +/- 25 min/24 h. Treatment with propranolol and nifedipine resulted in reduction of episodes and duration of painful and painless ischemia; approximately 77% of patients were free of all ischemic episodes. It is concluded that patients with chronic stable mild angina have a low incidence of silent ischemia. Nifedipine or propranolol alone, titrated to individualized maximally tolerated dosages, are equally effective in long-term control of painful and painless ischemia, anginal episodes and exercise-induced ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Proarrhythmic effects of antiarrhythmic drugs during programmed ventricular stimulation in patients without ventricular tachycardia.

The proarrhythmic effects of class IA antiarrhythmic drugs were prospectively evaluated during programmed ventricular stimulation in 24 consecutive patients with frequent ventricular premature beats whose baseline study, performed while no antiarrhythmic drugs were being taken, showed no inducible sustained ventricular arrhythmias. No patient had nonsustained (greater than 5 beats) or sustained ventricular tachycardia by history or baseline 24 hour ambulatory electrocardiographic monitoring. Sequential stimulation studies using up to three extra-stimuli were performed after administration of procainamide, quinidine and disopyramide on different days. Proarrhythmic response was defined as induction of one or more of the following: sustained monomorphic ventricular tachycardia; sustained polymorphic ventricular tachycardia; ventricular fibrillation; reproducibly inducible nonsustained monomorphic ventricular tachycardia. During 55 antiarrhythmic drug trials (24 of procainamide, 21 of quinidine, 10 of disopyramide) in the 24 patients, 6 patients had a proarrhythmic response: sustained monomorphic ventricular tachycardia in 3, ventricular fibrillation in 2, nonsustained monomorphic ventricular tachycardia in 1. Thus, 11% of drug trials resulted in a proarrhythmic response and 25% of patients had a proarrhythmic response to one of the drugs tested. A proarrhythmic response to one drug did not predict a similar response to another drug of the same class. The 6 patients with a proarrhythmic response did not differ significantly from the other 18 patients with regard to underlying heart disease, electrocardiographic or baseline 24 hour ambulatory electrocardiographic characteristics; however, they did have a higher incidence of digoxin usage (p less than 0.02), a shorter baseline right ventricular effective refractory period (p less than 0.01) and a smaller increment in effective refractory period during antiarrhythmic drug testing (p = 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Early tolerance to hemodynamic effects of high dose transdermal nitroglycerin in responders with severe chronic heart failure.

Transdermal systems for delivery of nitroglycerin have been shown to provide sustained blood levels of the drug for at least 24 hours. Investigations of hemodynamic effects of transdermal nitroglycerin in patients with heart failure have demonstrated a transient reduction in pressure lasting less than the expected 24 hours. These findings could be due to the development of circulatory tolerance to the vasodilatory effects of nitroglycerin or to insufficient drug dosing. In the present study, we compared the hemodynamic effects of the first and the second doses of high dose (120 mg) transdermal nitroglycerin given 24 hours apart in 11 responders (greater than or equal to 20% reduction in mean pulmonary artery wedge pressure lasting greater than or equal to 2 hours). Initiation of nitroglycerin therapy resulted in a significant reduction in mean right atrial pressure lasting for 14 hours and in a reduction in mean pulmonary artery and mean pulmonary artery wedge pressures lasting 24 hours. After administration of the second dose, mean right atrial pressure at 2 hours (9 +/- 5 versus 7 +/- 4 mm Hg), 4 hours (8 +/- 5 versus 6 +/- 4 mm Hg) and 8 hours (8 +/- 5 versus 6 +/- 3 mm Hg) was higher than after the first dose (p less than 0.05). Both mean pulmonary artery and mean pulmonary artery wedge pressures were significantly higher after the second nitroglycerin dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Outcomes 15 years after valve replacement with a mechanical versus a bioprosthetic valve: final report of the Veterans Affairs randomized trial.

OBJECTIVES: The goal of this study was to compare long-term survival and valve-related complications between bioprosthetic and mechanical heart valves. BACKGROUND: Different heart valves may have different patient outcomes. METHODS: Five hundred seventy-five patients undergoing single aortic valve replacement (AVR) or mitral valve replacement (MVR) at 13 VA medical centers were randomized to receive a bioprosthetic or mechanical valve. RESULTS: By survival analysis at 15 years, all-cause mortality after AVR was lower with the mechanical valve versus bioprosthesis (66% vs. 79%, p = 0.02) but not after MVR. Primary valve failure occurred mainly in patients <65 years of age (bioprosthesis vs. mechanical, 26% vs. 0%, p < 0.001 for AVR and 44% vs. 4%, p = 0.0001 for MVR), and in patients > or =65 years after AVR, primary valve failure in bioprosthesis versus mechanical valve was 9 +/- 6% versus 0%, p = 0.16. Reoperation was significantly higher for bioprosthetic AVR (p = 0.004). Bleeding occurred more frequently in patients with mechanical valve. There were no statistically significant differences for other complications, including thromboembolism and all valve-related complications between the two randomized groups. CONCLUSIONS: At 15 years, patients undergoing AVR had a better survival with a mechanical valve than with a bioprosthetic valve, largely because primary valve failure was virtually absent with mechanical valve. Primary valve failure was greater with bioprosthesis, both for AVR and MVR, and occurred at a much higher rate in those aged <65 years; in those aged > or =65 years, primary valve failure after AVR was not significantly different between bioprosthesis and mechanical valve. Reoperation was more common for AVR with bioprosthesis. Thromboembolism rates were similar in the two valve prostheses, but bleeding was more common with a mechanical valve.

Renal hemodynamic effects of vasodilation with nifedipine and hydralazine in patients with heart failure.

The central and renal hemodynamic effects of nifedipine were evaluated in nine patients with severe chronic congestive heart failure. Oral nifedipine (34 +/- 22 mg, mean +/- standard deviation) was associated with a decrease in systemic vascular resistance from 1,748 +/- 436 to 1,321 +/- 302 dynes . s . cm-5 (p less than 0.001) and mean arterial blood pressure from 96 +/- 11 to 87 +/- 6 mm Hg (p less than 0.05) and with an increase in cardiac output from 4.2 +/- 1.1 to 4.9 +/- 1.2 liters/min (p less than 0.001). Although renal vascular resistance decreased from 11,988 +/- 2,256 to 10,286 +/- 3,011 dynes . s . cm-5 (p less than 0.05), no significant change was seen in renal blood flow (599 +/- 120 to 640 +/- 162 ml/min), glomerular filtration rate (62 +/- 18 to 62 +/- 17 ml/min), filtration fraction (18 +/- 5 to 17 +/- 6%), the ratio of renal/systemic vascular resistance (7.0 +/- 1.0 to 7.9 +/- 1.8) and the ratio of renal blood flow/cardiac output (0.15 +/- 0.02 to 0.13 +/- 0.03). Intravenous hydralazine (10 +/- 5 mg), given to eight of the patients in a randomized crossover design, resulted in a larger increase in cardiac output than did nifedipine (38 +/- 7 versus 19 +/- 10%, p less than 0.001) and in an increase in total renal blood flow from 570 +/- 152 to 645 +/- 174 ml/min (p less than 0.001). Renal vascular resistance decreased from 12,080 +/- 2,934 to 10,153 +/- 2,372 dynes . s . cm-5 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiographic detection of pneumomediastinum and pneumopericardium: the air gap sign.

Six patients referred for echocardiographic evaluation in whom an unusual echocardiographic sign resulted from air within the mediastinum or pericardium are described. Three patients had a pneumomediastinum that occurred after chest trauma and three patients had a pneumopericardium induced during a therapeutic pericardiocentesis. Important features included a broad band of echoes (air) recorded during held respiration which obscured the normal cardiac structures and dropout (gap) of echoes posteriorly. Between the cyclic appearance of the "air gap" sign, intracardiac structures were normally visualized. Echocardiographic recording of the air gap sign was identical in the six cases; it disappeared after resolution of clinical signs and symptoms of the pneumopericardium or pneumomediastinum. The pattern most likely resulted from air within the anterior mediastinum or pericardium interfering with the echographic beam and resulted in a cyclic appearance from systole to early diastole as the air was displaced by the changing cardiac size. Recognition of the air gap sign can be helpful in evaluating patients for pneumomediastinum or pneumopericardium after thoracic trauma.

Mitral valve aneurysm: clinical features, echocardiographic-pathologic correlations.

Aneurysm of the mitral valve occurs most commonly in association with infective endocarditis of the aortic valve. The probable mechanism of its formation is destruction of the aortic valve which results in a regurgitant jet that strikes the anterior leaflet of the mitral valve, creating a secondary site of infection leading to the development of an aneurysm. Perforation of these aneurysms may occur, resulting in mitral regurgitation and pulmonary edema from a ventricle already volume overloaded from aortic regurgitation. This report describes the clinical and echocardiographic-pathologic findings in five patients with pathologically proven aneurysm of the mitral valve. There are no clinical features that appear specific for this abnormality. The two-dimensional echocardiographic feature that is helpful in the diagnosis is a bulge of the mitral valve leaflet toward the left atrium that persists throughout the cardiac cycle. Preoperative diagnosis is important because a mitral valve aneurysm may produce serious complications and is frequently overlooked during surgery. Repair of the aneurysm may be feasible; otherwise, valve replacement becomes necessary. Careful two-dimensional echocardiographic examination should be done in patients with left-sided infective endocarditis to detect an aneurysm of the mitral valve.

Day to day reproducibility of electrically inducible ventricular arrhythmias in survivors of acute myocardial infarction.

Day to day reproducibility of the response to programmed ventricular stimulation has not been evaluated in survivors of acute myocardial infarction. Programmed ventricular stimulation was performed prospectively on 2 consecutive days in 56 patients on an average of 12 +/- 5 days (range 7 to 29) after an acute myocardial infarction. No patient had a history of documented or suspected sustained ventricular tachycardia or fibrillation occurring greater than 48 h after infarction. During initial programmed ventricular stimulation, 21 patients had induction of sustained ventricular tachycardia or fibrillation (Group I), and 35 patients had induction of either nonsustained ventricular tachycardia or no ventricular tachycardia (Group II). Repeat programmed ventricular stimulation in Group I patients induced sustained ventricular tachycardia or fibrillation in 16 of 21 patients (reproducibility 76%); the maximal induced response in the other 5 patients was nonsustained ventricular tachycardia in 2 patients and fewer than six repetitive ventricular responses in 3 patients. The day to day reproducibility was significantly higher for inducible sustained ventricular tachycardia of cycle length greater than or equal to 240 ms compared with rapid sustained ventricular tachycardia of cycle length less than 240 ms (100% versus 44%, p less than 0.009) or ventricular fibrillation (100% versus 43%, p less than 0.009). Repeat programmed ventricular stimulation in Group II patients did not induce sustained ventricular arrhythmias in 31 of 35 patients (reproducibility 89%). Thus, in survivors of acute myocardial infarction, inducible slow sustained ventricular tachycardia was a highly reproducible finding, whereas inducibility of rapid sustained ventricular tachycardia and ventricular fibrillation showed a significant day to day variability.(ABSTRACT TRUNCATED AT 250 WORDS)

Left main coronary artery spasm. A potential cause for angiographic misdiagnosis of severe coronary artery disease.

Two patients had catheter-induced spasm of the left main coronary artery during diagnostic coronary arteriography. One patient had no coronary artery disease, and the other had minimal disease of the right coronary artery. Spasm was relieved by nitrates; however, in one patient several doses were needed over 35 minutes. Catheter-induced spasm must be considered in the diagnosis of left main coronary artery disease, particularly on a patient with isolated left main coronary artery disease.

Survival in patients with intraventricular conduction defects.

All 42,000 electrocardiograms taken at the University of Oregon Health Sciences Center from 1969 through 1971 were reviewed; 325 patients (0.77%) had left bundle-branch block (LBBB) or right bundle-branch block (RBBB) with axis deviation (AD). In December 1974, 90% were contacted or found to be dead. The five-year survival rate (actuarial technique) (mean +/- SE) was 45.5 +/- 2.9%. It was significantly worse than that of age- and sex-matched "controls." In most patients the cause of death could not be determined. Survival of 164 LBBB patients (40.7 +/- 4.1%) at five years was not significantly worse than that of 161 RBBB and AD patients (49.5 +/- 4.2%). Those with syncope did no worse in terms of survival than did those without. The five-year survival in coronary artery disease patients was 33.7 +/- 4.4%, in those with primary conduction system disease (20% of patients), it was 50.6 +/- 6.6%. It will be necessary to know the causes of death and of syncope in conduction disease patients before it can be determined whether or not pacemakers can prevent either.

Left ventricular performance after acute myocardial infarction. Sectrum of functional abnormalities and importance of wall motion disturbances during convalescent phase.

Seventeen patients underwent catheterization of the right and left sides of the heart and left ventricular (LV) angiography three to six weeks after acute myocardial infarction. Fourteen of 17 patients had abnormal LV function. Three patients had altered LV diastolic properties; five patients had abnormalities of diastolic properties and of systolic function; and six patients had abnormal systolic function, but diastolic function could not be assessed. Thirteen of the 14 patients with abnormal LV function had LV wall motion abnormalities, which were quantitatively related to impaired LV systolic function.

Multiple bilateral myxomas demonstrated by two-dimensional echocardiography.

The two-dimensional and M-mode echocardiographic detection of multiple atrial myxomas is described in an asymptomatic patient with a family history of myxomas. Surgery was subsequently performed without resort to cardiac catheterization studies. Echocardiographic techniques correctly delineated the number and size of the tumors, as well as their site of attachment, mobility and degree of interference with cardiac function.

Detection of acute myocarditis using nuclear magnetic resonance imaging.

The clinical features, echocardiographic characteristics, and electrocardiographic findings in two patients with acute myocarditis are presented. The first patient had rheumatic myocarditis and the other had probable viral myocarditis. Both patients had regional wall motion abnormalities on the echocardiogram, and the nuclear magnetic resonance image for each patient showed myocardial edema in the area of the wall motion abnormality. These changes disappeared with resolution of the acute disease process. These preliminary data indicate that nuclear magnetic resonance imaging may show myocardial edema in acute myocarditis.

Left atrial transport function in myocardial infarction. Importance of its booster pump function.

After myocardial infarction (MI), left ventricular (LV) end-diastolic pressure (EDP) is higher than mean pulmonary artery wedge pressure because of powerful atrial contraction. To evaluate the significane of atrial contraction to left ventricular function we studied 10 control (C) patients without cardiac disease and 17 patients from three to six weeks after acute myocardial infarction. Cardiac catheterization with simultaneous left ventricular diastolic pressure (DP) and left ventricular cineangiograms were obtained. Left ventricular volumes and pressure were (mean +/- SD): (SEE ARTICLE). Although left ventricular stroke volume was lower in the patients with myocardial infarction than in the control subjects (46 versus 56 ml/m2), atrial contraction contributed more to left ventricular filling during diastole (which is the same as left ventricular stroke volume) in the patients with myocardial infarction than in the controls (16 versus 10 ml/m2). The average atrial contribution to left ventricular end-diastolic volume was 11.9 per cent (C), 15.4 per cent (MI); to left ventricular end-diastolic pressure 20 per cent (C), 38.7 per cent (MI); and to left ventricular stroke volume 21.7 per cent (C), 35.1 per cent (MI). Atrial contribution to left ventricular stroke volume was 56 per cent in patients with a cardiac index less than or equal to 2.0 liters/min/m2 and 31 per cent in those with a cardiac index greater than 2 liters/min/m2 (p less than 0.01). Atrial contraction contributed 35 per cent to left ventricular stroke volume in patients with normal end-diastolic volume and in those with increased end-diastolic volume and 10 per cent to end-diastolic volume in patients with increased end-diastolic volume (p less than 0.001). In patients with myocardial infarction, atrial contraction made a large contribution to left ventricular filling and stroke volume irrespective of the type of left ventricular functional derangement that was present. The "booster pump" function of the atrium cannot be ignored in assessing left ventricular performance.

From coronary artery disease to heart failure: role of the hibernating myocardium.

Hibernating myocardium is defined as persistently impaired myocardial and left ventricular (LV) function at rest resulting from reduced myocardial blood flow. It may occur in unstable angina and chronic stable angina, acute myocardial infarction, and LV dysfunction and congestive heart failure. Recovery of the hibernating myocardium has clearly been shown to occur with the establishment of successful revascularization either by coronary bypass surgery or by percutaneous transluminal coronary angioplasty. It may be possible to show recovery of the viable myocardium by reducing myocardial oxygen demand and/or by increasing coronary blood flow with pharmaceutical agents.