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Postreperfusion regional myocardial dysfunction may be associated with depletion of high energy phosphate compounds during ischemia and with their relatively slow repletion during reperfusion. However, few studies have correlated relatively rapid changes in regional myocardial function (sonomicrometers) and blood flow (microspheres) with high energy phosphate concentrations measured using phosphorus-31 nuclear magnetic resonance spectroscopy in intact large animal models of regional myocardial ischemia. The left anterior descending coronary artery of mongrel dogs was abruptly occluded for 17.1 ± 1.9 minutes and then completely released; measurements were made for an additional 22 minutes. Transmural blood flow decreased from 1.07 ± 0.25 to 0.25 ± 0.10 ml/(min × g) and holosystolic expansion was observed in all dogs (segmental systolic shortening decreased from 9.3 ± 3.7 to −6.3 ± 6.0%). Phosphocreatine (PCr) measured during 4.4 minute sampling intervals decreased to steady state within the first sampling period after occlusion and was 45.9 ± 17.0% of control at the end of the occlusion, whereas beta-adenosine triphosphate (beta-ATP) reached its lowest level early after reperfusion (72.7 ± 13.3% of control). The ratio of PCr to inorganic phosphate (Pi) decreased during the occlusion (3.34 ± 0.75 versus 1.01 ± 0.61) but returned to control level early during reperfusion. The ratio of PCr to beta-ATP also decreased during coronary occlusion (2.16 ± 0.39 versus 1.29 ± 0.39) but did not return to control level during reperfusion.

The usefulness of end-systolic measures of ventricular function was compared with that of standard contractility indexes in conscious dogs. End-systolic relations between left ventricular pressure and volume and between pressure and wall thickness were analyzed in dogs previously instrumented with ultrasonic crystals. Progressive angiotensin infusions were used to generate computer-averaged pressure-volume and pressure-wall thickness loops. Both relations were linear in every study and highly reproducible.

Some studies have reported increased short-term mortality and higher incidence of multivessel coronary artery disease in patients with inferior myocardial infarction and complete heart block, but information is lacking on clinical outcome after hospital discharge. Therefore, data were obtained and analyzed in 749 patients who were admitted with inferior myocardial infarction to four different centers and followed up for 1 year. Six hundred fifty-four patients (Group 1) did not have complete heart block and 95 (Group 2) had complete heart block during their hospital stay (incidence rate 12.8%).

Prognostic differences between patients with anterior or inferior myocardial infarction are often related to such variables as previous infarction or the size of the myocardial infarct. We examined the determinants of mortality in 997 hospital survivors of acute Q wave infarction (anterior in 449, inferior in 548) who, although not preselected, were well matched with respect to age, sex and prior infarction or congestive heart failure. Additionally, there was no significant difference in peak serum creatine kinase (CK) between the groups with anterior and inferior infarction (1,459 ± 1,004 versus 1,357 ± 1,036).

The administration of digitalis glycosides causes a variety of extracardiac effects. In both normal human subjects and in other species, digitalis increases smooth muscle tone of resistance and capacitance vessels. The vasoconstriction is mediated, in part, by a direct action of these glycosides on smooth muscle and, in part, by an increase in alpha-adrenergic tone. Constriction of coronary and splanchnic vessels may lead to myocardial or mesenteric ischemia. In contrast to normal subjects, patients with congestive heart failure demonstrate arteriolar and venodilation in response to these glycosides, possibly because the myocardial effect, to increase cardiac output and peripheral blood flow, overcomes the vasoconstrictor properties of these drugs. Other important actions of digitalis glycosides occur in the central and peripheral nervous systems. Their effects on the area postrema of the medulla oblongata are largely responsible for the alpha-adrenergic-mediated peripheral vasoconstriction, as well as the nausea and vomiting that frequently accompany digitalis intoxication. Actions of glycosides on the cerebral cortex are responsible for the wide range of neurotoxic effects that range from visual disturbances and headaches to seizures and coma. Finally, peripheral neurologic effects of digitalis glycosides on baroreceptor and cardiac afferent fibers may: 1) improve the depressed function of these receptors in the situation of heart failure, and 2) reflexly lower peripheral vascular resistance, thereby partially preventing the vascular constrictor action of these glycosides.

In the management of patients with valvular heart disease, an understanding of the effects of altered loading conditions on the left ventricle is important in reaching a proper decision concerning the timing of corrective operation. In acquired valvular aortic stenosis, concentric hypertrophy generally maintains left ventricular chamber size and ejection fraction within normal limits, but in late stage disease function can deteriorate as preload reserve is lost and aortic stenosis progresses. In this setting, even when the ejection fraction is markedly reduced (< 25%), it can improve to normal after aortic valve replacement, suggesting that afterload mismatch rather than irreversibly depressed myocardial contractility was responsible for left ventricular failure. Therefore, patients with severe aortic stenosis and symptoms should not be denied operation because of impaired cardiac function.

Two-dimensional and Doppler echocardiography were performed in 17 consecutive hospitalized patients with cystic fibrosis aged 6 to 38 years (mean 21 ± 9) and in 10 normal subjects aged 24 ± 7 years. Left ventricular and right ventricular ejection fraction were measured by a computerized light pen system and Simpson's rule from two-dimensional echocardiographic apical four and two chamber views. Right ventricular wall thickness, inferior vena cava size and the presence of tricuspid regurgitation by Doppler recording were also assessed. National Institutes of Health (NIH) score of clinical severity ranged from 22 to 72 (mean 51 ± 15) (100 = excellent, 0 = poor). Four patients, all with an NIH score of 40 or less, died of respiratory failure within 1 year of the echocardiographic study.

Doppler echocardiography was performed in 136 patients with a normally functioning prosthetic valve in the aortic (n = 59), mitral (n = 74) and tricuspid (n = 3) positions. These included patients with St. Jude (n = 82), Björk-Shiley (n = 18), Beall (n = 13), Starr-Edwards (n = 7) or tissue (n = 16) valves. Peak and mean pressure gradients across the prostheses were measured using the simplified Bernoulli equation. The prosthetic valve orifice (PVO, in square centimeters), only in the mitral position, was calculated by the equation: PVO = 220/pressure half-time.

Tricuspid regurgitation is often not apparent on physical examination and several methods are now available to aid in this difficult assessment. Cardiac catheterization using right ventriculography, previously considered the diagnostic standard, has several limitations. Currently available noninvasive tools such as M-mode and two dimensional echocardiography (with or without contrast), Doppler techniques and even radionuclide cardiologic imaging have added significantly to the precise assessment of the presence and severity of tricuspid regurgitation. This review examines the comparative use and limitations of these various techniques.

The relation among right ventricular preload, afterload and ejection fraction in patients with mitral valve disease has not been well elucidated. In this study, measurements were made of intracardiac pressures and forward cardiac output during cardiac catheterization (n = 43), the ejection fraction by radionuclide angiography (n = 43) and end-systolic radius and wall thickness by Mmode echocardiography (n = 22). There was a linear correlation between pulmonary artery pressure and right atria] pressure (r = 0.57, p < 0.01). The right ventricular peak circumferential systolic wall stress was increased in 68% of the patients (in comparison with wall stress measurements obtained in 10 normal subjects). The right ventricular ejection fraction was abnormal in 38 patients (88%) and abnormal in 14 of the 15 patients with high wall stress. There was an inverse correlation between ejection fraction and end-diastolic volume (r = -0.61, p p < 0.001). The right ventricular ejection fraction measurement was repeated within 3 months after mitral valve replacement in 16 patients; the ejection fraction increased from 21 ± 9 to 29 ± 10% (mean ± standard deviation) after surgery (p < 0.01), but normalization of the ejection fraction was observed in only 3 patients (19%).

Because previous reports have suggested that digitalis administration may lead to increased mortality after hospital discharge for acute myocardial infarction, the independent importance of digitalis therapy in long-term prognosis after acute myocardial infarction was investigated by analyzing 1,599 patients after definite myocardial infarction. After hospital discharge, mortality rate for the entire group at 4 months was 7.7% and after 1 year 14.2%. At discharge, 36.6% of the patients were taking digitalis. Compared with those not taking digitalis, those taking digitalis had more historical risk factors and a higher incidence of important clinical prognostic variables during the hospitalization. Their cardiac mortality rate after 4 months and 1 year (12.5 and 22.4%, respectively) was significantly higher than that of patients not taking digitalis (5.0 and 9.6%, respectively). Mortality was higher for patients taking digitalis whether or not they had congestive heart failure during hospitalization. However, in a multivariate Cox analysis for 1 year outcome, neither digitalis nor any other medication variable displaced the important clinical variables of age, congestive heart failure during the hospitalization, previous myocardial infarction, maximal heart rate during the hospitalization and previous angina. Quinidine and digitalis at discharge were selected sixth and seventh (not significant) by the analysis.

Left ventricular hypertrophy is an important adaptive response to chronic pressure or volume overload of the left ventricle. The different types and the pathophysiologic mechanisms of the development of left ventricular hypertrophy in various disease states are reviewed. Detection of left ventricular hypertrophy may be accomplished by electrocardiography and cardiac angiography. Echocardiography, however, is the most accurate noninvasive method to detect the presence and estimate the severity of increased left ventricular mass. The clinical significance of left ventricular hypertrophy and its prognostic implications in several cardiac diseases as- sociated with hypertrophy are discussed. The critical transition stage from adaptive, compensatory and reversible left ventricular hypertrophy to “pathologic” hypertrophy with impaired left ventricular contractility and irreversible myocardial damage is yet unknown.

Noninvasive techniques are helpful in evaluating the function of mechanical prostheses and tissue valves. Combined phonocardiography and M-mode echocardiography together with cinefluoroscopy are the most useful noninvasive techniques in differentiating normal from abnormal metallic prosthetic valve function. The intensity of the opening and closing clicks and associated murmurs will depend on the type of prosthetic valve, the heart rate and rhythm and the underlying hemodynamic status. Arrhythmias or conduction disturbances, or both, may produce motion patterns that mimic some of the echocardiographic signs of malfunctioning prosthetic valves. Differentiation of thrombus formation or tissue ingrowth from paravalvular regurgitation or dehiscence is possible by noninvasive techniques. Disc variance, a potentially serious and lethal problem with the older Beall valves, can be readily detected by cinefluoroscopy and echophonocardiography.

Several noninvasive techniques, including radionuclide angiography and Doppler echocardiography, have attempted to measure the regurgitant volume in patients with mitral regurgitation; however, none of these techniques are entirely satisfactory. Utilizing a computerized light pen method for tracing the left atrial endocardial border during systole and diastole in two orthogonal planes (apical four and two chamber views), biplane volume determinations were calculated in 12 normal subjects and 30 patients with nonrheumatic mitral regurgitation. Left atrial emptying volume determinations were performed by subtracting the left atrial end-diastolic volume from the left atrial end-systolic volume. The degree of mitral regurgitation was visually assessed as normal (0, trivial, Group I, 12 patients), mild (1 +, Group II, 4 patients), moderate (2 + , Group III, 8 patients), moderately severe (3 + , Group IV, 12 patients) and severe (4 +, Group V, 6 patients) by contrast left ventricular angiography and also quantitatively by regurgitant fraction at cardiac catheterization.

M-mode and Doppler echocardiography were performed in 16 patients with first degree atrioventricular (AV) block, 1 patient with second degree (Werickebach type) and 3 patierits with third degree AVblock; 20 individuals with a hormal PR interval served as control subjects. The time from the onset of the P wave to the mitral valve closure by M-mode and to the end of mitral flow by Doppler echocardiography were obtained. In 20 normal subjects, the P wave to niitral valve closure interval measured 220 ± 30 ms by M-mode and to the end of mitral flow 225 ± 29 ms by Doppler technique (p = NS). In patients with first degree AV block, these intervals measured 242 ± 41 and 249 ± 36 ms, respectively (p = NS).

The purpose of this study was to test the hypothesis that moderately severe exercise-induced regional myocardial ischemia can be prevented by combined pharmacologic intervention. Eight chronically instrumented dogs were studied using an ameroid constrictor to produce critical stenosis of the left circumflex coronary artery. The dogs were studied during steady state treadmill exercise that induced regional myocardial dysfunction (reduced systolic wall thickening; sonomicrometers) and ischemia (reduced subendocardial blood flow; microspheres). During a control exercise run, wall thickening in the ischemic posterior wall decreased from 21.4 to 13.3% whereas subendocardial blood flow failed to increase normally (36% of that in the normal zone). In the control anterior wall, both wall thickening and subendocardial blood flow increased significantly during the control run. Wall thickness-left ventricular pressure loop areas were calculated as an index of regional work; this index increased abruptly with the onset of exercise in both regions but became significantly depressed in the ischemic region during the steady state exercise.

Doppler echocardiography was performed in 80 consecutive patients (22 men, 58 women), aged 38 ± 16 years, who had mitral valve prolapse diagnosed by two-dimensional echocardiography. Of the 80 patients, 16 (20%) were asymptomatic and 11 (14%) had a normal physical examination (no click or murmur). The M-mode echo, cardiogram was negative for mitral valve prolapse in 11 patients (14%) and equivocal or nondiagnostic in 19 patients (24%). Mitral regurgitation was evaluated using pulsed mode Doppler echocardiography and was quantified by the mapping technique as minimal or mild when a holosystolic regurgitant jet was recorded just below the mitral valve into the left atrium, and as moderate or severe when the jet was detected at the mid- or distal left atrium.

The onset and resolution of electrical and functional measures of regional myocardial ischemia were examined in nine conscious dogs during control exercise and exercise after beta-receptor blockade. The dogs had been instrumented with an ameroid constrictor and were studied when no regional dysfunction was evident at rest, although severe coronary stenosis or coronary occlusion with collateral circulation development was present. ST segment elevation was measured on subendocardial electrograms, and regional wall motion was studied by sonomicrometry. During control exercise, subendocardial myocardial blood flow in the ischemic zone, normalized to blood flow in the nonischemic zone, decreased. Subendocardial ST elevation increased slowly, was significantly different from control standing values by 2.5 minutes of exercise and returned quickly to control values within 5 minutes after exercise. Percent systolic wall thickening decreased rapidly, was significantly depressed by 1 minute of exercise and did not return to control values until 30 minutes after exercise.

Two-dimensional echocardiographic determination of right ventricular ejection fraction was compared with right ventricular ejection fraction obtained by first pass radionuclide angiography in 39 patients with coronary artery disease. Apical four chamber and two chamber right ventricular views were obtained in 34 (87%) of the 39 patients, while a subcostal four chamber view was obtained in 31 patients (80%). Right ventricular ejection fraction by two-dimensional echocardiography was calculated by the biplane area-length and Simpson's rule methods using two paired orthogonal views and utilizing a computerized light-pen method for tracing the right ventricular endocardium. A good correlation (r = 0.74 to 0.78) was found between radionuclide angiographic and two-dimensional echocardiographic right ventricular ejection fraction for each method used. Patients with acute inferior myocardial infarction had the lowest right ventricular ejection fraction by radionuclide angiography and two-dimensional echocardiography (p < 0.05 compared with patients with right coronary artery obstruction and no infarction). There were no differences in right ventricular ejection fraction between patients with acute and old inferior myocardial infarction by both techniques. No correlation was found between left and right ventricular ejection fraction by radionuclide angiography (r = 0.16).

Improved understanding of cardiac muscle and whole heart function has substantially benefited clinical diagnosis and therapy. Knowledge of the influence of systolic loading conditions has been of key importance in these advances, and the role of peripheral circulatory responses is beginning to be appreciated. Dissociations between myocardial contractility and cardiac function are described, including acute heart failure due to afterload mismatch associated with normal myocardial contractility, and normal ventricular function associated with depressed contractility in chronic mitral regurgitation. Frameworks for assessing cardiac and myocardial function are examined. Standard invasive and noninvasive approaches can now be usefully supplemented by end-systolic pressure-volume and end-systolic wall stress-volume frameworks, the former being particularly useful for analyzing the concept of "afterload mismatch with limited preload reserve" and the latter being useful for studying chronic cardiac adaptations. The clinical importance of systolic loading conditions and venous return is illustrated within these frameworks by a description of responses to a vasopressor stress test to produce an apparent descending limb of left ventricular function, the concept of steady state afterload mismatch in chronic and acute heart failure and the responses to vasodilator therapy in the normal and failing heart. The importance of changes in venous return in determining the cardiac output response to a vasodilator, in addition to the effects of reduced afterload on the ventricles, is emphasized. Finally, the problem of assessing left ventricular function in patients with chronic mitral regurgitation is examined and, for the patient with severe mitral regurgitation and few symptoms, tentative guidelines for recommending operation to avoid irreversible left ventricular dysfunction postoperatively are presented.

One hundred twenty-six patients with a St. Jude valve prosthesis were followed up clinically and studied by combined M-mode echocardiography and phonocardiography. Fifty patients underwent aortic valve replacement, 58 underwent mitral valve replacement and 18 underwent a combination of the two. The early postoperative mortality rate was 8% for aortic, 6.9% for mitral and 6% for combined valve replacement. Followup ranged from 2 to 46 months (mean ± SD 28 ± 9). The late postoperative mortality rate was 5%; in patients who survived, improvement in New York Heart Association functional class occurred in 97%. Major thromboembolic events occurred in two patients and antico-agulation-related complications occurred in three patients.

Whether ventricular fibrillation occurring within 48 h after acute myocardial infarction is associated with particular clinical features and poor prognosis, especially in patients with anterior myocardial infarction, is still debated. Therefore, clinical variables and in-hospital and 1 year mortality rates were analyzed in 2,088 patients, aged 18 to 95 years (mean ± SD 64 ± 12), admitted to the hospital with acute myocardial infarction between 1979 and mid 1984. One hundred forty-seven patients (7%) had at least one episode of ventricular fibrillation occurring within 48 h of hospital admission. Of these, 25% died during their initial hospitalization compared with 13% of patients without early ventricular fibrillation (p < 0.001). In >50% of patients with early ventricular fibrillation, the immediate cause of death was left ventricular failure or cardiogenic shock.