Theodore L. Biddle

Comparison of intravenous milrinone and dobutamine for congestive heart failure secondary to either ischemic or dilated cardiomyopathy

Milrinone and dobutamine are positive inotropic agents with beneficial hemodynamic effects in patients with congestive heart failure. This study was undertaken to compare the effects of intravenous milrinone and dobutamine in patients with stable New York Heart Association class III or IV congestive heart failure and to test the hypothesis that intravenous milrinone is at least as beneficial as dobutamine in this setting. Seventy-nine patients were randomized to either dobutamine therapy at incremental doses of 2.5, 5, 7.5, 10, 12.5 and 15 micrograms/kg/min, or milrinone as a bolus of 50 or 75 micrograms/kg followed by an infusion of 0.5 to 1.0 micrograms/kg/min. Both agents significantly increased heart rate, cardiac index and stroke volume index and decreased pulmonary artery wedge pressure and systemic vascular resistance compared with baseline levels (p less than 0.01). During sustained infusion for 48 hours, no difference in hemodynamic effects was observed between the 2 drugs. Ventricular tachycardia occurred in 5 patients (3 taking milrinone, 2 taking dobutamine); 1 patient taking milrinone had ventricular fibrillation. Milrinone and dobutamine elicited similar beneficial hemodynamic results with relatively few adverse effects.

Effect of furosemide on hemodynamics and lung water in acute pulmonary edema secondary to myocardial infarction

Hemodynamic studies were carried out in 19 patients with left ventricular failure complicating acute myocardial infarction. Fourteen patients were studied before and after the intravenous administration of 0.5 mg/kg of furosemide, and five patients served as a control group. Serial measurements included intracardiac pressures, cardiac output and lung water by a double isotope technique. A significant reduction was noted in right atrial (P less than 0.005), pulmonary arterial (P less than 0.0005) and pulmonary wedge pressures (P less than 0.0005) after administration of furosemide. Only the change in right atrial pressure was significantly different from that in the control group (P less than 0.05). Lung water was not changed in 4 patients studied 2 hours after administration of furosemide but was significantly changed in the remaining 10 patients studied 4 to 24 hours after furosemide (P = 0.0001). This change was also significantly different from values in the control group (P less than 0.05). The patients with no reduction in excess lung water also had a smaller reduction in pulmonary wedge pressure and a lower pretreatment stroke work index than the other patients. The mobilization of excess lung water in patients with acute myocardial infarction complicated by left ventricular failure has several features. Despite a prompt diuresis, the reduction in lung water is delayed for at least several hours after the administration of furosemide and may be related to the degree of left ventricular dysfunction. Venodilation may be a major result of treatment with furosemide.

ST-segment variations after acute myocardial infarction. Relationship to clinical status.

SUMMARY The degree of vectorcardiographic ST-sgment elevation was employed as an index of myocardial ischemic injury in a study of 27 patients after acute myocardial infarction (AMI). The ST-segment vector magnitude (STVM) was derived from the continuously recorded modified Frank vectorcardiogram and was plotted serially by hours after onset of AMI. The STVM in normal subjects was 51.1 ± 7.1 μV (mean ± SE). A standard deviation of the pooled variance of 15.2 1iV was obtained in a group of control patients and a change of more than 2 SD (> 30 μV) in an individual STVM was considered to be significant. The STVM progressively decreased in patients who survived without clinical complications while it remained elevated in those with congestive heart failure. A modest, sustained re-elevation of STVM was observed in patients who developed pericarditis, and a significant late average increase of 64 μV occurred in survivors with infarct extension. In contrast, STVM underwent a major increase in patients who died. In five of these six patients without associated pericarditis a mean increase of 164 μV was recorded in the last 5–12 hours of life. While death was clinically predictable in two patients with cardiogenic shock, it was not so for the four other patients who died. Thus, major increases in STVM frequently suggested significant new ischemic injury and were often premonitory to sudden death after AMI. The increases preceding death implied that not only ventricular ectopy but also lethal conduction abnormalities after AMI might be ischemia-related.

Lung Water in Patients with Acute Myocardial Infarction

Pulmonary extravascular water volume (PEV) or lung water was measured in 45 patients with acute myocardial infarction, utilizing the double radioisotope indicator dilution technique. A PEV greater than the upper limit or normal (120 ml/m2) was found in 27 patients, 23 of whom had an elevated pulmonary wedge or pulmonary artery diastolic pressure. A significant correlation was found between PEV and pulmonary wedge or pulmonary diastolic pressure in the whole series. A progressive increase in average PEV was observed from Class I (uncomplicated) to Class IV (shock) patients. There was also a progressive increase in PEV from patients with normal chest X-ray findings to those with radiologic evidence of acute pulmonary edema. In seven of 11 patients with initial elevation of both PEV and pulmonary wedge pressure, repeat determinations demonstrated a substantial reduction in both parameters over a period of 2-4 days.We postulate that an increased PEV in patients with acute myocardial infarction is largely due to an elevated pulmonary capillary pressure. The latter is probably a consequence of an elevated left ventricular diastolic pressure, which may be a manifestation of either left ventricular failure or a decrease in left ventricular compliance.

Measurement of S-T segment elevation in acute myocardial infarction in man: Comparison of a precordial mapping technique and the frank vector system

Precordial S-T segment mapping has been used to evaluate the extent of ischemic injury in patients with acute myocardial infarction. Because precordial S-T segment mapping is time-consuming and is limited to patients with anterior wall myocardial infarction, we evaluated the possibility of using the magnitude (ST-VM) and direction (ST-VD) of the S-T vector, derived from X, Y and Z leads of the Frank vector system, as a substitute for the precordial S-T segment mapping technique. Precordial S-T segment mapping and Frank system vectorcardiograms were simultaneously obtained in three groups: (1) nine normal subjects; (2) nine patients with persistent S-T segment elevation 2 to 15 months after acute anterior myocardial infarction; and (3) nine patients with acute anterior myocardial infarction studied on 41 occasions. For both systems the S-T segments were analyzed 20 and 60 msec after completion of inscription of the QRS complex. The sum of the S-T segment elevations for the 35 sites (sigma ST) and the number of sites (NST) in which S-T segment elevations exceeded 0.1 mv were computed for the precordial S-T maps. The ST-VM and ST-VD were calculated by standard formulas from X, Y and Z lead tracings of the Frank vector system. Good correlations were observed between: ST-VM and sigma ST (r = +0.818 and +0.791 at 20 and 60 msec, respectively, P less than 0.001); and ST-VM and NST (r = +0.773 and +0.705 at 20 and 60 msec, respectively, P less than 0.001). Furthermore, changes in the location of S-T segment elevations in serial precordial S-T segment maps were reflected by changes in ST-VD. Observations in patients with inferior wall myocardial infarction suggest that ST-VM and ST-VD can be serially followed in such patients. Thus, estimation of the magnitude and direction of the S-T vector is a simple alternative to standard precordial S-T segment mapping that allows for continuous monitoring of S-T segment elevations in all patients with acute myocardial infarction.

Relation of Heart Block and Left Ventricular Dysfunction in Acute Myocardial Infarction

Two hundred one patients with acute transmural myocardial infarction were studied to determine the relation of heart block and the degree of left ventricular dysfunction. Right bundle branch block occurred in 17, left bundle branch block in 7 and either left anterior or left posterior hemiblock in 8 patients. Hemodynamic studies were carried out before heart block developed. Complete heart block occurred in 9 of 92 patients with diaphragmatic (inferior) myocardial infarction and in 6 of 109 with anterior infarction. In patients with diaphragmatic infarction who experienced complete heart block hemodynamic measurements before block did not differ significantly from those in patients without block. Similarly, in patients who had right bundle branch block or hemiblock the hemodynamic variables did not differ from those in patients without bundle branch block. In patients with anterior infarction who experienced complete heart block, however, stroke index ( P P P P Although only a small number of patients with heart block were studied, careful analysis of the clinical and hemodynamic data support the findings.

Relationship of serum and myocardial digoxin concentration to electrocardiographic estimation of digoxin intoxication.

Serum and myocardial digoxin levels were studied in 18 patients who came to autopsy. An independent analysis of electrocardiograms prior to death was made to ascertain the relationship between serum and tissue levels of digoxin and clinical estimation of drug toxicity. Patients with arrhythmias of digoxin toxicity had higher mean serum and tissue digoxin levels than patients without arrhythmia. There was overlap in the patient groups, however, and the differences were not statistically significant. The tissue to serum ratio was lower in the toxic patients. The latter phenomenon is unexplained but may be related to decreased tissue binding.

Ventricular arrhythmias and cardiac hemodynamics in patients with myocardial infarction. Comparison of the acute and post-hospitalization phases

Sixty-six patients with myocardial infarction (MI) were studied during the acute hospital phase and during the six months after hospital discharge. The clinical characteristics, location of infarction, and data from right heart catheterization were studied in an attempt to determine what factors were associated with ventricular rhythm disturbance. Those patients with serious ventricular arrhythmias (SVA) in the acute phase of infarction were found to have a significantly greater degree of myocardial dysfunction as measured by pulmonary artery and pulmonary wedge pressure than patients with more normal rhythm (p less than .05). Clinical classification of patients and location of infarction were not helpful in predicting SVA during the acute infarction period. Knowledge of hemodynamic data, presence of SVA and clinical characteristics in the acute infarction period were of no value in predicting the occurrence of SVA after hospital discharge patients having had an acute diaphragmatic infarction were found to have a higher incidence of SVA after hospital discharge.