Some applications of the concept of body forces for the myocardium.
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Biomedical subjects
Publications and source records attributed to J Rouleau.
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Three series of investigations were carried out with prazosin (PZN) hydrochloride. In the first, hemodynamic effects of PZN were compared with those of hydralazine (HDZ) in 11 patients with chronic congestive heart failure (CHF). In doses up to 5 mg, PZN increased cardiac output (CO) 20% accompanied by a 20% decrease in pulmonary capillary wedge pressure (LVFP). HDZ increased CO by 50% with little or no effect on LVFP. An additional 12 patients were given multiple 5 mg doses of PZN at 6-hour intervals with measurements of hemodynamic and plasma blood levels. Results suggested an attenuation of the effects of PZN on increasing CO but not on decreasing LVFP. This attenuation of CO was not due to inadequate plasma levels. Acute exercise studies (supine bicycle) were performed in 10 patients with severe CHF before and after the administration of several doses of PZN. There appeared to be a greater effect of PZN during exercise than at rest, with a beneficial increase in CO and reduction in LVFP. These data suggest that, despite hemodynamic attenuation of its effects on CO at rest, PZN may still be beneficial to active patients with CHF. In vitro studies with various vasodilators were performed to evaluate potential intropic effects. Isometric force (cat papillary muscle) increased 2% with 10-4M and 31% with 10-3M HDZ. PZN increased force 4% at 10-6M and 18% at 10-4M. Captopril did not increase force development at any dose level. The doses of HDZ and PZN that increased force development were higher than usual clinical doses.
We investigated the effect of hypercholesterolemia on coronary and cardiac hemodynamic responses to intracoronary norepinephrine (NE) (0.01 to 10.0 micrograms/min as the bitartrate) in a Gregg cannula autoperfusion system. Coronary blood flow was measured by the radioactive microsphere technique in two groups of open-chest dogs anesthetized with pentobarbital: 10 controls and 8 that were fed a cholesterol-rich diet (CD) which doubled the serum cholesterol level. In the control dogs, NE in doses of 0.01 to 1.0 micrograms/min had no effect on coronary vascular resistance (CVR) but 10 micrograms/min caused a significant decrease to 0.58 +/- 0.12 of control. In the CD dogs, NE at doses of 1.0 and 10.0 micrograms/min significantly reduced CVR, to 0.72 +/- 0.06 and 0.52 +/- 0.11 of control, respectively. There was no consistent effect of NE, at these doses, on myocardial oxygen uptake, left ventricular stroke work index, or maximal positive dP/dt. In a second series of experiments we measured coronary flow with electromagnetic flowmeters in 11 chronically instrumented conscious dogs, 5 controls, and 6 CD. In the control dogs, intravenously administered NE hydrochloride, 0.01 microgram/min, reduced CVR to 0.74 +/- 0.07 of control, and 1.0 microgram/min increased CVR to 1.26 +/- 0.09 of control. In the CD animals, these effects were seen at a 10-fold lower NE dose, 0.001 microgram/min (0.83 +/- 0.11 of control) and 0.1 microgram/min (1.32 +/- 0.06 of control). The vasodilation was blocked by propranolol, and vasoconstriction by phentolamine. We conclude that NE at low doses activates beta-adrenoreceptors to reduce CVR and at higher doses activates alpha-adrenoreceptors to increase CVR; the vasoconstrictor response is inhibited in pentobarbital anesthetized dogs, and hypercholesterolemia sensitizes coronary vessels to both the dilator and constrictor effects of NE.
The present study attempts to verify the relative efficacy of two forms of pre-exposure which are identical in content and parallel in mode of exposure (in vivo or videotape). These two forms of pre-exposure were given to 38 children, aged four to six years old, before their first dental visit. The results showed that all groups manifested relatively little negative behavior while seeing the dentist. The theoretical and methodological implications of this study are discussed.
The postpericardiotomy syndrome occurs in 10% to 40% of patients who undergo open-heart surgery. Its frequency is reportedly decreased when pericardial drainage is used. To challenge this, 50 consecutive patients (1 was disqualified) were randomly assigned to two groups: one in which only the anterior mediastinum was drained (group 1) and the other in which the anterior mediastinum and posterior pericardium were drained (group 2). The surgical procedures performed were: coronary artery bypass grafting in 14 patients, valve surgery in 23 and repair of congenital defects in 12. The two groups were similar with respect to age and the volume of blood drained. Significant differences were found only for the duration of bypass and volume of blood given. At 7 to 10 days there were no differences in the frequency of fever, thoracic pain or presence of arthralgia. Findings were similar in both groups for leukocyte count, sedimentation rate, serum lactic dehydrogenase value and for the frequency of positive blood, urine and sputum cultures. Six patients (three in each group) had a postpericardiotomy syndrome that required steroid treatment and prolonged hospitalization for 10 more days. However, none had postpericardiotomy syndrome complicating coronary artery bypass surgery. None of the patients had cardiac tamponade. This study demonstrates that pericardial drainage has no effect on the frequency of postpericardiotomy syndrome and appears to be unnecessary after open-heart surgery.
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The sensitivity of myocardial perfusion imaging (MPI) using thallium-201 injected both at rest and during peak exercise was compared to simultaneously recorded 12 lead electrocardiography (ECG) for the detection of transient ischemia in 20 normal subjects and 63 patients with coronary artery disease (CAD). No significant perfusion defects or ECG changes were seen on either the rest or exercise studies in any of the normal subjects. Fifty-six percent of patients with CAD developed new perfusion defects with exercise compared to 38% who developed ischemic ST-segment depression (P less than 0.02). However, when chest pain and/or ST depression were considered indices of ischemia, the sensitivity of exercise testing and thallium-201 MPI was similar. The increased sensitivity of MPI compared to ST-segment depression on the ECG was due to patients with baseline ECG abnormalities and those who failed to achieve 85% of predicted maximum heart rate with exercise. Analysis of the exercise results according to the extent of coronary artery disease revealed a progressive increase in both positive ECGs and MPI with the number of vessels involved. In patients with single vessel disease the MPI was more sensitive than the ECG (P less than 0.02). The combination of the rest and exercise ECG, MPI and chest pain during exercise failed to identify 11% of patients with CAD. Exercise thallium-201 MPI is a useful adjunct to conventional exercise testing particularly when evaluating patients with abnormal resting ECGs, those who develop ventricular conduction defects of arrhythmias during exercise, and those who fail to achieve their predicted heart rate because of fatigue or breathlessness.
The value of myocardial scanning with 43K was assessed in 64 consecutive patients undergoing coronary arteriography, and in five young volunteers. Myocardial scans at rest detected only 16 of the 35 transmural infarcts documented on electrocardiograms, 11 of 11 anterior infarcts and five of 24 in other sites. Myocardial scans were obtained immediately after a graded exercise test in the five normal volunteers, in nine patients with normal coronary arteriograms and in 25 patients with atherosclerotic narrowing greater than 75% involving the left anterior descending artery, with or without disease of other coronary vessels. All patients with normal coronary arteriograms had normal myocardial scans. A regional perfusion deficit was observed after exercise in all six patients with single vessel disease, but in only 11 of the 19 patients with disease involving two or three vessels. Although the technique was specific, it lacked sensitivity, due mostly to poor resolution and the location of the disease.
It has been shown previously that 30-minute infusions of intravenous nitroglycerin in patients with acute myocardial infarction are able to lower left ventricular filling pressure and improve left ventricular function while lowering mean arterial pressure by only 7 mmHg (0.9 kPa). A decrease in sigmaST in praecordial ST segment mapping studies during nitroglycerin infusion in patients with anterior infarction suggested a decrease in the extent of myocardial ischaemia. In the present study, 30 patients with acute myocardial infarction received 1- to 3-hour infusions of intravenous nitroglycerin at infusion rates sufficient to lower mean arterial pressure by an average of 22 mmHg (2.9 kPa). An improvement in ventricular function was noted in that subgroup of patients with the msot severe left ventricular dysfunction. All patients with anterior myocardial infarction underwent serial ST segment mapping and, irrespective of the presence or absence of left ventricular failure, showed a decrease in sigmaST during nitroglycerin infusion (P less than 0.005). These findings suggest that infusion of nitroglycerin improves left ventricular function and/or alters left ventricular compliance in patients with left ventricular failure complicating myocardial infarction and furthermore decreases sigmaST in all patients, irrespective of the presence or absence of left ventricular failure, suggesting that the extent of myocardial ischaemia is decreased.
Eleven patients with a clinical diagnosis of bacterial endocarditis underwent scintillation scanning of the precordial region 2-7 days after the intravenous administration of 3 mCi of gallium-67 citrate. Seven had positive scans, 3 of which were confirmed by postmortem imaging at autopsy. Serial images revealed the scans to be frequently negative at 48 hours and positive from 3 to 8 days following injection. Uptake was not seen in the region of the myocardium 48 hours or longer after the injection of 15 patients without endocarditis used as controls.
Thallium-201 myocardial perfusion images were obtained from 13 healthy adults after tracer administration both at rest and at maximal stress. On the rest-injected scan, tracer was seen in left ventricular myocardium, liver, and spleen. In two subjects with resting tachycardia, the right ventricular myocardium was slightly visualized after tracer injection at rest. When tracer was administered at stress, the left ventricular activity was more nearly homogeneous and the left ventricle was better defined on the scan. The left-ventricle-to-lung-background activity ratio increased from 2.4 at rest to 3.4 at stress. The right ventricular myocardium was seen on the stress-injected scan. Phantom studies, performed to define the optimum position for visualization of lesions, showed that small lesions were best defined when seen either en face or in tangent. Scans should be performed at stress whenever possible and multiple views are essential.
To determine whether thallium 201 myocardial imaging could be used to detect hypertrophic cardiomyopathy, 10 patients with idiopathic hypertrophic subaortic stenosis were studied. Asymmetric septal hypertrophy, an anatomic marker for this disease, was evident on thallium scans in the patients with idiopathic hypertrophic subaortic stenosis, with a ratio of septum to left ventricular free wall of 1.7 cm compared to 1.0 cm in eight normal volunteers, and 1.0 cm in eight patients with concentric left ventricular hypertrophy. Patients with hypertrophic cardiomyopathy also demonstrated apical ventricular wall thickening, and a thicker posterior ventricular free wall in the obstructive in contrast to the nonobstructive form of this disease. Thallium scans of three patients with pulmonary hypertension and secondary asymmetric septal hypertrophy were distinguished from idiopathic hypertrophic subaortic stenosis by marked right ventricular wall thickening. Thus, thallium 201 myocardial perfusion imaging provides a noninvasive method for detection and evaluation of idiopathic hypertrophic subaortic stenosis.
Abnormalities of left ventricular function and extent of myocardial infarction were studied in relation to prevalence of late ventricular premature contractions (VPCs) in 36 patients in the convalescent stage of acute myocardial infarction (MI). Left ventricular ejection fraction (EF) and percent akinesis (%A) were calculated from gated cardiac blood pool scans; myocardial infarct size was estimated from peak CPK values; and VPCs were detected by 24 hour ambulatory ECGs 2-4 weeks following hospitalization for acute MI. Twenty-two patients had either zero (class 0) or less than 30/hour unifocal VPCs (class I). Fourteen patients had greater than 30/hour unifocal (class II), multifocal (class III) or coupled VPCs (class IV), including ventricular tachycardia. Thirteen of 14 class II-IV patients had EF less than 40% compared with only 8 of 22 class 0-I patients. Class II-IV patients had significantly lower mean EF (30.5 +/- 2.3 SE to 49.6 +/- 4.0) P less than 0.01, higher mean %A (28.1 +/- 2.2 to 16.9 +/- 3.7) P less than 0.05, and higher mean peak CPK (1350 +/- 187 to 721 +/- 155) P less than 0.05 than class 0-I patients. These data suggest that VPCs may not be an independent risk factor for sudden cardiac death in the convalescent phase of MI.
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Twenty-seven patients with suspected acute myocardial infarction were studied by precordial scanning after intravenous administration of 99mTc-gluchoheptonate 2-48 hr after the onset of chest pain. Fifteen of the patients had clinically documented acute myocardial infarctions. Twelve of these 15 (80%) had areas of distinctly increased tracer uptake in the region of the heart. The three infarctions not identified by scan had peak serum CPK values of less than 300. In seven patients without infarction, no distinct areas of increased tracer uptake were found in the region of the heart. Five patients could not be classified as to whether infarction had or had not occurred. Three had abnormal scans, the significance of which is uncertain. Infarct size was estimated from the area of increased 99mTc-glucoheptonate concentration on scan and compared to peak serum CPK values. A linear correlation with a correlation coefficient of 0.77 was found. Technetium-99-m-glucoheptonate scanning was useful for the identification and size estimation of moderate- to large-size transmural and nontransmural acute myocardial infaractions.
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