Henry S. Loeb

Comparative responses to dobutamine and nitroprusside in patients with chronic low output cardiac failure.

The acute hemodynamic effects of dobutamine and nitroprusside were compared in 19 patients with low output cardiac failure. At dosage levels yielding similar increases in cardiac index (12 patients), nitroprusside resulted in significantly lower arterial systolic and wedge pressures and did not increase heart rate suggesting advantages over dobutamine when reduction in myocardial oxygen requirement or pulmonary congestion is a major goal. Systemic arterial mean and diastolic pressures were minimally changed with dobutamine, but fell significantly with nitroprusside suggesting advantages of dobutamine over nitroprusside in patients where hypotension could limit coronary blood flow or perfusion of other vital organs. Reduction in pulmonary arteriolar resistance occurred only with nitroprusside. Arterial hypoxemia developed in three patients during nitroprusside infusion suggesting the possibility of increased right-to-left intrapulmonary shunting resulting from a direct vasodilating effect of nitroprusside on pulmonary arteriole smooth muscle. Although both inotropic and vasodilator drugs can result in hemodynamic improvement when administered to patients with chronic low output cardiac failure, significant differences of potential clinical importance exist between these two modes of therapy.

Effects of pharmacologically-induced hypertension on myocardial ischemia and coronary hemodynamics in patients with fixed coronary obstruction.

Twenty patients with fixed coronary artery obstruction were studied during rapid atrial pacing and methoxamine infusion. During pacing to heart rates of 142 ± 4 (mean ± SEM) beats per minute coronary sinus flow increased from 108 ± 8 to 187 4 15 cc/min and myocardial oxygen consumption increased by + 80 + 11%. During methoxamine infusion that raised arterial systolic pressure to 196 i 5 mm Hg, similar increases in coronary sinus flow (to 179 i 13 cc/min) and myocardial oxygen consumption (+ 77 i 12%) occurred. Chest pain and ischemic ST segment changes developed in 17 and 14 patients respectively during atrial pacing, an incidence significantly greater (P < 0.05) than during infusion of methoxamine (6 and 3 patients). Myocardial lactate extraction which averaged 26 i 4% during control was decreased to 10 + 8% during pacing and to 24 ± 7% during methoxamine; the difference between decreases was not significant. The data show that at similar increases in myocardial oxygen consumption stress of increased heart rate results in more myocardial ischemia than stress of increased afterload.

Hemodynamic effects of intravenous phentolamine in low output cardiac failu;e. Dose-response relationships.

Nineteen patients with chronic low output cardiac failure were studied before, during and after infusion of phentolamine in doses of 10, 20, 30 and 40 microgram/kg/min. Significant reduction of left- and right-sided pressures and increases in cardiac index and heart rate (HR) were present within 15 minutes of starting phentolamine at the 10 microgram/kg/min dose. Minimal additional effect was observed at 30 minutes. Increased dose from 10 to 20 mu/kg/min resulted in small but significant (P less than 0.05) additional reduction in pressures and increases in HR. No additional significant changes occurred at doses of 30 or 40 microgram/kg/min. Significant hemodynamic changes persisted for at least an hour (53 +/- 3 min) after the phentolamine infusion was discontinued. Near maximal ;emodynamic effects occur within 15 minutes of starting phentolamine infusion and can be achieved at doses of 10 to 20 microgram/kg/min. Increased HR during phentolamine infusion may limit its usefulness in patients with ischemic heart disease.

Beneficial effects of dopamine combined with intravenous nitroglycerin on hemodynamics in patients with severe left ventricular failure.

Hemodynamic effects of dopamine and intravenous nitroglycerin alone, and in combination, were studied in 27 patients with severe left ventricular failure. Dopamine alone increased cardiac index from 1.8 to 2.5 l/min/m2 but also increased wedge pressure from 24 to 30 mm Hg and heart rate from 88 to 101 beats/min. Arterial oxygen saturation fell from 92% to 87% (p less than .001). Nitroglycerin alone had a lesser effect on cardiac index (1.8 to 2.2 l/min/m2) but decreased wedge pressure from 26 to 16 mm Hg and heart rate from 91 to 86 beats/min. Arterial oxygen saturation fell from 91% to 90% (NS). Combined dopamine and nitroglycerin administration resulted in optimal hemodynamics, with cardiac index of 2.9 l/min/m2, wedge pressure of 17 mm Hg, and heart rate of 96 beats/min. Arterial oxygen saturation remained low at 88% in spite of the reduction in left ventricular filling pressure, which probably reflects increased intrapulmonary right-to-left shunting coupled with increased pulmonary blood flow. These results suggest that the combination of dopamine with intravenous nitroglycerin should be considered for patients with severe left ventricular dysfunction who require temporary pharmacologic support.

Improved survival after surgical therapy for chronic angina pectoris: one hospital's experience in a randomized trial.

SUMMARY Between 1972 and 1974, 121 patients with chronic stable angina pectoris and operative coronary artery disease, excluding significant left main coronary obstruction, were randomized to either medical therapy (60 patients) or surgical therapy (61 patients) as part of a larger Veterans Administration Cooperative Study of Surgery for Coronary Arterial Occlusive Disease. At the time of randomization, medical and surgical groups were similar with regard to clinical and hemodynamic features as well as degree of left ventricular impairment and extent of coronary disease. Follow-up to June 1, 1978, reveals significantly improved survival in surgical patients from 3 through 6 years after randomization. Sixteen cross-over patients (13 medical to surgery, and 3 surgical without surgery) do not appear to influence results. Results of this randomized study from a single hospital differ from the preliminary results of the larger cooperative study, primarily because of a higher mortality in the medical group. The medical mortality in our group is in keeping with other reports of the natural history of patients with angina pectoris, and we propose that the population of patients we randomized closely simulates the usual type of patient with chronic angina being considered for surgical treatment. Our good surgical results thus contrast significantly with the survival of medically treated patients, and this separates our study from the body of the Veterans Administration Cooperative Study.

Effects of low-dose dobutamine on coronary hemodynamics, myocardial metabolism, and anginal threshold in patients with coronary artery disease.

Fourteen patients with coronary artery disease and normal or near-normal left ventricular function were studied at rest and during atrial pacing until the occurrence of angina (12 patients) before and during infusion of dobutamine (3.80 +/- 0.45 micrograms/kg/min). At rest, during the infusion, three patients developed chest pain, mean ST segment depression increased from 0.02 to 0.08 mV (p less than .001), and myocardial lactate extraction fell from +17.5% to -1.4% (p less than .05). These ischemic changes were associated with significant increases in arterial systolic pressure (134 to 149 mm Hg), heart rate (79 to 91 beats/min), coronary sinus flow (89 to 113 ml/min), and myocardial oxygen consumption (10.8 to 13.5 cc/min). In contrast, during atrial pacing, dobutamine did not reduce the pacing threshold or further increase myocardial oxygen consumption or ST segment changes; however, arterial mean and diastolic pressures were significantly lower with pacing during dobutamine infusion compared with control pacing. In the absence of heart failure, dobutamine in low doses can cause myocardial ischemia in patients with coronary artery disease. The absence of increased ischemia from dobutamine during pacing may reflect reversal of pacing-induced ventricular dysfunction.

The effects of right atrial and ventricular pacing on the auscultatory findings in patients with mitral valve prolapse.

Fifteen patients with midsystolic clicks associated with mitral valve prolapse were studied in order to assess changed in ausculatatory findings produced by pacing-induced variations in cardiac rate, rhythm, and conduction. As the heart rate was increased in stepwise intervals to the maximum possible extent by right atrial pacing (RAP) in 14 patients, the interval between the Q wave and the click (Q-C) decreased in all cases (21 plus or minus msec/10 beats/min; P smaller than 0.001). In two patients, RAP at rates of and above 118 and 159 per minute, respectively, resulted in disappearance of the click. During right ventricular pacing (RVP) without evidence of atrioventricular (A-V) dissociation on the surface ECG in ten patients, the click was inaudible at all pacing rates in three instances. In all seven of the cases in which the click was audible at the lowest rate of RVP with VA conduction, Q-C was greater and C-S2 less than that in sinus rhythm. As the rate of RVP was increased, Q-C was noted to decrease (26 plus or minus 4 msec/10 beats/min) and C-S2 to increase (19 plus or minus 7 msec/10 beats/min) in all patients. In three patients in whom RVP induced atrioventricular dissociation, the click was seen only in beats closely preceded by a P wave. In ten of 11 patients the click occurred earlier in systole with a postextrasystolic or post tachycardia beat as compared to its appearance after a sinus beat when a shorter preceding diastolic filling period was present (P smaller than 0.001). In the eleventh patient a loud systolic murmur was present during a postextrasystolic cycles. It is concluded that pacing-induced rhythm disturbances can result in disappearance of a midsystolic click or can alter its timing and cause it to mimic sonic phenomena seen in other disease states. The possibility of similar changes taking place as a result of spontaneously occurring disturbances of rate, rhythm, and conduction should be recognized in order that the possible diagnosis of mitral valve prolapse not be overlooked.

Regional diastolic functional images utilizing time-domain analysis of gated radionuclide ventriculograms

Early quantitative investigations of left ventricular function concentrated primarily on the systolic portion of the cardiac cycle. Recent studies suggest that signs and symptoms in cardiac failure previously attributed to impaired systolic performance may be due in part to altered diastolic properties of ventricular function,1-3 and that abnormalities in diastolic performance may appear earlier than do systolic abnormalities.“, 5 Thus, altered diastolic function may be a significant early indicator of coronary disease. Radionuclide gated blood pool ventriculography has been shown to be useful for assessing ventricular function. Initially, analysis consisted of the visual inspection of a closed loop cinematic presentation, permitting easy comparison with radiographic contrast ventriculograms. Advanced techniques now employ computerized mathematical models to analyze various aspects of regional ventricular performance through the use of parametric images derived from the composite frame data. Typically, one fits a mathematical function, defined by one or more parameters, to the time-activity curve of each picture element (pixel) of the digitized study. A parametric, or functional, image is formed by displaying a value at each pixel location corresponding to the value of the parameter associated with the time-

Assessment of Ventricular Function after Acute Myocardial Infarction by Plasma Volume Expansion

In order to see if changes in preload could be used to help assess left ventricular function, 24 patients with uncomplicated acute myocardial infarction (AMI) received plasma volume expansion (PVE). In eight patients (group A) cardiac index (CI) increased by 20% or more, and in 16 patients (group B) CI increased by less than 20% or decreased. By plotting left ventricular stroke-work index (LVSWI) against left ventricular end-diastolic pressure (LVEDP) before and after PVE, the ventricular function curves upon which the heart was operating could be assessed. In group A patients the values moved upward and to the right, while in group B the values during PVE moved horizontally or downward and to the right suggesting that at rest these hearts were operating at the peak of their function curves.Patients in group B had a higher incidence of anterior infarction and a lower control mean arterial pressure than patients in group A, but other clinical and control hemodynamic values did not differ between the two groups. Follow-up data suggest that patients in group B may have had a higher mortality within the first 6 months following AMI.Changing preload by PVE appears to be a safe and potentially useful means of assessing ventricular function following AMI and deserves further study.

The mechanism and significance of ventricularization of intracoronary pressure during coronary angiography

Ventricularization of pressure during coronary angiography has been said to identify the presence of left main coronary artery disease, but the hemodynamic features and the mechanism of this process have not been studied. Twenty consecutive patients with ventricularization were identified prospectively in our laboratory. Four patients had a discrete ostial left main stenosis and 16 patients had stenosis of the entire length of the left main coronary artery. The degree of pressure drop upon cannulation of the diseased left main coronary artery was highly variable; the systolic pressure decreased by 9 to 94 mm Hg, and the diastolic pressure decreased by 6 to 60 mm Hg. The morphology of the ventricularized pressure was distinct. It had a presystolic deflection resembling an a wave. The upstroke of this waveform was slower and the downstroke was steeper than that of the aortic pressure. An identical waveform was observed in dogs after partial occlusion of the left main coronary artery with a balloon-tipped catheter. The waveform of the so-called ventricularized pressure is derived from the aortic pressure, which is altered by its transmission across the left main coronary stenosis. The appearance of ventricularization is an important clue to the presence of left main coronary artery disease.