Interventricular septal motion and left ventricular function after coronary bypass surgery: evaluation with echocardiography and radionuclide angiography.

To evaluate interventricular septal motion and left ventricular function after coronary bypass graft surgery, 40 patients were studied early postoperatively and serially for up to 16 months with echocardiography and radionuclide angiography. Early after operation mean left septal excursion decreased significantly from 4.6 +/- 0.4 (standard error) to 0.8 +/- 0.6 mm (P less than 0.001), and left septal motion was abnormal in 23 of the 40 patients. Mean right septal excursion reversed from 2.1 +/- 0.5 to -2.1 +/- 0.5 mm early after operation in the 22 patients in whom these measurements could be made, and 15 patients showed paradoxical right septal excursion. At a mean of 4 months after operation, only 7 of 35 patients followed up had abnormal left septal motion, and mean left septal excursion had returned toward normal (3.6 +/- 0.7 mm); mean right septal excursion remained reversed (--1.1 +/- 0.7 mm), and 6 of the 14 patients followed up had paradoxical motion. In the 22 patients whose wall thickness could be measured, mean septal thickening during systole decreased significantly from 35 +/- 4 to 21 +/- 3 percent early after operation (P less than 0.01). During late follow-up septal thickening returned toward normal (32 +/- 4 percent). Mean normalized posterior wall velocity increased significantly after operation from 0.76 +/- 0.03 to 1.01 +/- 0.05 sec-1 (P less than 0.001), but posterior wall thickening remained unchanged. Left ventricular end-diastolic dimension and the radionuclide-determined left ventricular ejection fraction were unchanged postoperatively. It is concluded that (1) echocardiographically detected abnormal septal movement is frequent early after coronary bypass graft operation; (2) both decreased myocardial contraction in the septum and increased anterior movement of the whole heart contribute to this abnormality; (3) the abnormalities in septal movement decrease during late follow-up in many patients but persist in some patients; and (4) posterior wall function tends to increase early after operation and therefore overall left ventricular function remains normal.     

Combined hyertrophic subaortic stenosis and calcific aortic valvular stenosis.

A well documented case of combined hypertrophic subaortic stenosis and calcific aortic stenosis is reported. Detection of multilevel involvement in cases of left ventricular outflow obstruction requires a high index of suspicion and precise hemodynamic and angiographic documentation. Careful analysis of the total data base is necessary for proper management of the patient. The pathogenesis of this combined lesion is unclear: Asymmetrical septal hypertrophy may occur as a consequence of the valvular stenosis, or it may be that abnormal leaflet motion in patients with hypertrophic obstruction produces leaflet thickening, calcification, deformity and stenosis.     

Effects of changes in preload,afterload and inotropic state on ejection and isovolumic phase measures of contractility in the conscious dog

Despite much investigation, the usefulness of various indexes employed clinically for detecting alterations in ventricular contractility in the intact circulation remains controversial. The effects of acute preload, afterload and contractility changes on both ejection and isovolumic phase measures of left ventricular function were analyzed in normal, trained conscious dogs instrumented with micromanometers and endocardial ultrasonic diameter gauges. Rapid volume overload increased the excursion of the left ventricular diameter (Δ LVD) by 7 percent above the control level, but mean velocity of circumferential shortening (V_CF) did not change significantly; peak rate of left ventricular pressure rise (dP/dt) increased by 11 percent and (dP/dt)/DP40 (DP = developed pressure) was augmented by 10 percent, but maximal [(dP/dt)/LVP], or “V_pm” decreased by 20 percent. Pressure overload by phenylephrine infusion decreased Δ LVD by 15 percent and mean V_CF fell by 26 percent; peak dP/dt and (dP/dt)/DP40 remained unaltered, but V_pm was reduced by 37 percent. Isoproterenol augmented peak dP/dt by 55 percent, and (dP/dt)/DP40, V_pm and mean V_CF were increased comparably. Propranolol decreased these measures equally by about 16 percent. Therefore, in the conscious animal in the steady state, isovolumic phase indexes were mildly influenced by acute volume loading, whereas ejection phase indexes were not. Acute increases in aortic pressure markedly reduced ejection phase measures, whereas the isovolumic indexes were unaffected. All of the indexes studied were comparably sensitive to acute alterations in contractility, but we conclude that no single measure can always be used for defining an acute contractility change in the intact circulation.     

Phosphorylase kinase mediating the effects of cyclic AMP in muscle.

In the classic view of the control of phosphorylase b to a conversion by catecholamines, cyclic AMP acts as the second messenger stimulating the activity of cyclic AMP-dependent protein kinase to covalently modify phosphorylase kinase. Phosphorylation of phosphorylase kinase converts this enzyme form with a nonactivated to an activated form with a markedly higher activity at pH 7. There is now considerable evidence that the activity of phospphorylase kinase is also regulated by changeds in the Ca-2+ concentration. The activity of both nonactivated and activated phosphorylase kinase is stimulated by Ca-2+ in the range of concentrations that have been reported to occur in the sacroplasm of contracting muscle, with the activated pphosphorylase kinase having a lower K-alpha for Ca-2+. Thus there are at leaset two mechanisms for the regulation of phosphorylase kinase activity in muscle. These mechanisms may act independently or in concert in controlling glycogenolysis stimulated by catecholamines, anoxia, or tetanic electrical stimulation...     

Prediction of late mortality after myocardial infarction from variables measured at different times during hospitalization

The long-term prognostic importance of sets of variables from different times in the hospital course after acute myocardial infarction was examined in 818 patients discharged from the hospital. Cardiac mortality during the first year after discharge was 11.1 %. For the end point death within 1 year after admission, discriminant function analysis identified 5 important factors from the history and the first 24 hours of hospitalization: maximal level of blood urea nitrogen, previous myocardial infarction, age, displaced left ventricular apex (abnormal apex) on physical examination, and sinus bradycardia (negative correlation). When data from the entire hospitalization were included, extension of infarction and maximal heart rate were also selected. When variables obtained at discharge were included, only the presence of S₃ gallop and abnormal apex were selected. In subgroups of patients, neither the left ventricular ejection fraction nor the presence of complex ventricular arrhythmias during a 24-hour ambulatory monitoring were independent predictors. Correct prediction was similar for each analysis, with 55 to 60% of the deaths and 79 to 81 % of survivors correctly identified. The high-risk group consisted of 25 % of the patients with 28 to 30 % predictive value for death in the first year. In conclusion, outcome up to 1 year after acute myocardial infarction can be predicted early after admission. Addition of more information later during the hospitalization and at discharge did not improve correct prediction and may be redundant for prognostic evaluation.     

Improvement by propranolol of regional myocardial dysfunction and abnormal coronary flow pattern in conscious dogs with coronary narrowing

The effects of propranolol on regional myocardial function and the pattern of coronary blood flow velocity were studied during partial coronary arterial constriction in conscious resting dogs. Miniature ultrasonic crystals were implanted subendocardially in the left ventricle for measurement of segment length in control and ischemic areas. Coronary blood flow was limited by inflation of an hydraulic-cuff around the left circumflex coronary artery to produce stable hypofunction in the ischemic segment. With coronary stenosis, which reduced mean flow by an average of 31 percent of the control value, the heart rate increased by 17 beats from 78 ± 4 beats/min (mean ± standard error of the mean) and the flow pattern changed from a dominant diastotic to a dominant systolic pattern (peak velocity ratio of systole to diastole, 0.35 ± 0.06 to 1.06 ± 0.09) without change in left ventricular systolic pressure. After administration of propranolol (0.5 mg/kg Intravenously), heart rate decreased to 72 ± 4 from 95 ± 4 beats/min and contraction in the Ischemic segment increased markedly, as did left ventricular wall thickening. Simultaneously, coronary flow returned to a normal velocity pattern. These favorable effects were only partially diminished by cardiac pacing to increase the heart rate to that before treatment with propranolol. This study provides evidence for a substantial beneficial effect of propranolol when myocardial dysfunction results from transient coronary arterial stenosis, and it suggests several mechanisms that may be operative under these conditions.     

Approach to the estimation of myocardial infarct size by analysis of precordial S-T segment and R wave maps

To assess the correlation of S-T segment elevations and the height of R waves of the precordial electrocardiogram with myocardial infarct size, we performed 35 lead precordial electrocardiograms (maps) in 24 patients with uncomplicated acute anterior transmural myocardial infarction. The initial analysis was carried out in 14 patients. Infarct size was estimated from the integration, from normal baseline to baseline, of serial serum creatine kinase (CK) values obtained at 2 to 4 hour intervals and expressed as IU/liter·hours. The first electrocardiographic maps were recorded 12 hours or less after the onset of symptoms. All S-T segment elevations and R waves were summed for each map (∑S-T and ∑R). There were positive correlations between the ultimate CK infarct size and the initially recorded ∑S-T (r = 0.69), the initially recorded log ∑R (r = ? 0.70) and the initial early decline in log ∑R per hour [(Δlog ∑R/Δhour)·10³, r = 0.88]. Therefore, these variables were combined in a multiple regression analysis; CK infarct size = 0.23 ∑S-T + 0.20 [(Δlog ∑R/Δhour)·10³]? 14.9 log ∑R + 36.8 (r = 0.97). In addition, on the basis of previous studies the initially recorded ∑S-T and log ∑R values were normalized with respect to time by calculating the expected ∑S-T value at 12 hours after the onset of symptoms (∑S-T₁₂) and the 12 hour interpolated values for ∑R (∑R₁₂). These values also showed a good correlation with infarct size: CK infarct size = 0.37 ∑S-T₁₂ + 0.16 [(Δlog ∑R/Δhour)·10³]^t- 18.2 log ∑R₁₂ + 40.4 (r = 0.97).To validate this approach, 10 additional patients were studied prospectively. Correlations between CK infarct size and the various measurements from the serial precordial maps were similar to those in the first study group, and CK infarct size correlated well with the electrocardiographic infarct estimates (r = 0.90 and r = 0.95, respectively). It is concluded that in selected patients CK infarct size can be directly related to the initial height of S-T segment elevations and the early rate of R wave decline and inversely related to later ∑R values, thereby providing a general approach for use in studies on the estimation of myocardial infarct size from precordial electrocardiographic maps.     

Improvement of exercise-induced left ventricular dysfunction with oral propranolol in patients with coronary heart disease.

The effect of propranolol on global cardiac function during exercise was analyzed with equilibrium fadionuclide angiography in 10 patients with ischemic heart disease. All patients had angina pectoris and S-T segment depression of more than 0.1 mv during treadmill exercise when not taking propranolol. Each patient was stressed with supine bicycle exercise to the same work load on a maintenance dose of propranolol (120 to 400 mg/day) and on a second occasion without the drug, the two tests being separated by an average of 16 days. The mean heart rate was reduced both at rest and during exercise after propranolol, but propranolol caused no significant reduction of the left ventricular ejection fraction at rest. In the study without administration of propranolol the average ejection fraction during exercise decreased from 0.56 ± 0.09 (standard deviation) to 0.50 ± 0.14. With propranolol, the ejection fraction was improved from the control value in every patient, the average value during peak exercise reaching 0.60 ± 0.15. Thus, the average ejection fraction increased by 22 percent (±12 percent) relative to the value during the same exercise without propranolol (P < 0.001). In 16 other patients with ischemic heart disease who did not take propranolol, reproducibility of the ejection fraction both at rest and at peak exercise on two occasions within 15 days was good (r = 0.95 and 0.97, respectively). It is concluded that oral propranolol therapy in patients with coronary artery disease can ameliorate left ventricular dysfunction induced by exercise and thereby may reduce myocardial ischemia.     

Survival after hospital discharge in matched populations with inferior or anterior myocardial infarction

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). Among the patients with anterior infarction who died during the 1 year follow-up period, 56% died in the first 60 days after hospital discharge compared with 18% of those without inferior infarction (p less than 0.01). Survival curves then became nearly identical at 3 months, and remained so until 1 year when the total mortality rate was 10% for the anterior and 7% for the inferior infarction group (p = NS). Variables associated with heart failure during the hospital phase were more prevalent in anterior infarction, but rales above the scapulae during the hospital stay (p less than 0.0001) and ventricular gallop at the time of discharge (p less than 0.0001) were the top two predictors of 1 year mortality by both univariate and multivariate analysis in inferior infarction. Age (p less than 0.0001) and peripheral edema (p less than 0.0001) were the strongest predictors of mortality in anterior infarction. Previous infarction, although just as common in the group with anterior infarction, was present at 1 year in 48% of nonsurvivors of the group with inferior infarction compared with only 19% of survivors (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiac function and myocardial contractility: a perspective

An experimental study was designed to validate postextrasystolic potentiation assessment of myocardial viability or functional reserve of cardiac segments after acute coronary occlusion. Segmental systolic fractional area changes and wall thickening in pacing-induced postextrasystolic beats were mapped in 12 closed chest dogs by two-dimensional echocardiography during a control period and from 20 minutes to 3 hours after occlusion of the left anterior descending coronary artery. The extent of myocardial ischemic and necrotic zones was evaluated in left ventricular slices and subsegements corresponding to echographic cross sections. During two-dimensional echocardiography, left ventricular segments that were found to be neither ischemic nor necrotic always exhibited a significant augmentation of both fractional area change and wall thickening during the postextrasystolic beat that followed an induced premature contraction with a 42.4% coupling interval. In segments without necrosis but with varying degrees of ischemia, significant postextrasystolic potentiation was also demonstrated, even after 3 hours of occlusion. In contrast, segments that developed more than 80% necrosis failed to potentiate systolic fractional area change after 2 hours, and systolic wall thickening, even after 20 minutes of coronary occlusion. Statistical evaluation revealed a characteristic threshold at 41 to 60% necrosis, beyond which no potentiation of function could be elicited 3 hours after occlusion. Extrapolation from the experimental data suggests that when two-dimensional echographic studies in myocardial ischemia indicate postextrasystolic augmentation of segmental left ventricular function, the latter segments may be assumed to contain only small infarcts or to consist of reversibly ischemic and normal myocardium. Conversely, segments that fail to exhibit postextrasystolic potentiation can be assumed to be more than 60% necrotic.     

Usefulness of preoperative and postoperative Tc-99m (Sn)-pyrophosphate scans in patients with ischemic and valvular heart disease.

To assess the usefulness of myocardial imaging with technetium-99m-stannous pyrophosphate for detecting acute myocardial necrosis in patients undergoind cardiac surgery, 66 such patients were stldied. Tc-99m (Sn)-pyrophosphate scans were obtained in all patients 3 to 6 days postoperatively and in 45 preoperatively. Electrocardiograms and serum samples for measuring myocardial isoenzyme of creatine kinase (MB CK) levels were obtained before and serially after cardiac surgery. Seven of the 46 patients undergoing myocardial revascularization had a definite new myocardial infarction as indicated by electrocardiogram and MB CK isoenzyme concentrations, and postoperative pyrophosphate scans were abnormal in all but one. In addition, six of the eight patients with possible myocardial infarction (elevated MB CK levels and persistent ST-T wave depressions) had an abnormal scan postoperatively. Seven of the 20 patients undergoing aortic or mitral valve replacement, or both, had a possible postoperative myocardial infarction by electrocardiogram and MB CK criteria and the myocardial scan was positive in two. All the patients with a normal electrocardiogram and normal MB CK levels had a normal pyrophosphate scan. Preoperative scans were obtained in 22 patients wit; valvular heart disease and were positive in two with a heavy calcified mitral valve on fluoroscopy and in one with a calcified aortic valve. After valve replacement, the pyrophosphate scan became normal in two patients and remained abnormal in the third patient with electrocardiograms and MB CK levels suggesting acute myocardial infarction. We conclude that the Tc-99m (Sn)-pyrophosphate scan is useful for analyzing the occurrence of acute myocardial infarction in patients undergoing cardiac surgery and that, in conjunction with the electrocardiogram, it permits confirmation or exclusion of that diagnosis. Furthermore, false positive pyrophosphate scans may occur in patients with heavy valve calcifications.