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Biomedical subjects

W B Hood

Publications and source records attributed to W B Hood.

At least 73 records · Page 4Linked to original sources
PubMed1978

The predictive value of anginal chest pain as an indicator of coronary disease during exercise testing.

To determine the significance of anginal chest pain during exercise testing, a series of 302 patients undergoing coronary arteriography with exercise testing was reviewed. Of the 302 patients, 85 had ischemic ECG changes and chest pain (Group I); 87 patients had ischemic ECG changes but no chest pain (Group II); 25 patients had chest pain but no ischemic ECG changes (Group III); 105 patients had neither chest pain nor ischemic ECG changes (Group IV). Coronary artery disease was present in 95% of Group I, 75% of Group II, 72% of Group III, and 28% of Group IV. Of those patients with coronary disease, multiple vessels were involved in 94% of Group I, 51% of Group II, 67% of Group III, and 21% of Group IV. The predictive value for presence and extent of coronary disease showed Group I greater than Groups II and III greater than Group IV (p less than 0.025). We conclude that (1) anginal chest pain during exercise testing predicts the presence and extent of coronary disease more accurately than its absence; (2) the presence of chest pain even without an ischemic ECG response during exercise testing appears to be as predictive of coronary disease as an ischemic ECG response alone; and (3) the combination of anginal chest pain during exercise testing and an ischemic ECG response is highly predictive of multivessel coronary artery disease.

Angina Pectoris↗
PubMed1978

Experimental myocardial infarction. XVI. The detection of inotropic contractile reserve with postextrasystolic potentiation in acutely ischemic canine myocardium.

Postextrasystolic potentiation after a single closely coupled extrasystole may identify residual ventricular contractile performance in acutely ischemic myocardium without producing sustained secondary ischemic depression of myocardial function. Postextrasystolic potentiation was systematically used in eight open chest dogs to assess the progression of regional contraction abnormalities during a 10 minute occlusion of the left anterior descending coronary artery. Segment function was determined from pressure-length loop areas inscribed during right ventricular pacing at 128 +/- 3 (mean +/- standard error of the mean) beats/min, and after single closely coupled (179 +/- 3 msec) extrasystoles. Despite a 50 percent decrease in border zone segment function, postextrasystolic potentiation consistently augmented mechanical performance to control levels throughout the ischemic period. Central ischemic zone segment function deteriorated more profoundly, with the development of holosystolic aneurysmal bulging within 30 seconds after occlusion. Nonetheless, postextrasystolic potentiation produced marked inotropic augmentation, but not to control levels, for up to 10 minutes of ischemia. These results suggest that latent viability and contractile reserve may exist during brief periods of coronary occlusion.

Animals↗
PubMed1978

Electrocardiographic mapping of the precordium in the coronary care unit.

Precordial electrocardiographic mapping systems comprising a large number of recording sites have been utilized in the Coronary Care Unit for following the natural course of ischemic injury and detecting extension of acute myocardial infarction in patients. These electrocardiographic techniques have also been found useful in evaluating the effects of a number of metabolic, hemodynamic and pharmacologic interventions currently proposed as effective means of reducing the extent of ischemic damage. However, these methods have not been found useful in the study of patients with inferior transmural or nontransmural myocardial infarctions. Bundle branch blocks and pericarditis complicating acute myocardial infarction invalidate the mapping technique. To assess effectiveness of therapeutic interventions, ST-segment changes taken as an index of ischemic injury are correlated with alterations of the QRS complex, used as a parameter of ischemic necrosis.

Coronary Care Units↗
PubMed1978

Mechanism of cardiac output response to hypertonic sodium chloride infusion in dogs.

Hypertonic sodium chloride and tris(hydroxymethyl)amino-methane (Tris) hydrochloride (0.3 mmol/kg.min) were infused intravenously into chloralose-anesthetized dogs over a 20-min period. Cardiac output, maximum left ventricular dP/dt, and (dP/dt)/P increased by 55, 33, and 23%, respectively, during NaCl infusion, but Tris HCl infusion had no effects. NaCl infusion did not change heart rate or left ventricular end-diastolic pressure. Mean systemic and pulmonry arterial blood pressures increased, whereas total peripheral and pulmonary vascular resistances decreased. Responsiveness of cardiac beta-adrenergic receptors, as determined by serial intravenous injections of epinephrine, was not affected by NaCl infusion. Plasma catecholamine concentration, however, increased during NaCl infusion. In addition, the increases in cardiac output, maximum left ventricular dP/dt and (dP/dt)/P were abolished by prior treatment with practolol, a cardioselective beta-adrenergic receptor blocking agent. These results suggest that the hemodynamic effects of NaCl infusion were caused, at least in part, by the inotropic action of catecholamines.

Animals↗
PubMed1978

Acute cardiac ischemia and reperfusion: contractility, relaxation, and glycolysis.

The mechanical and metabolic effects of 3 min of complete global ischemia and 25 min of reperfusion were studied in the isolated rat heart. The decrease in contracile function was biphasic; a rapid 50% decline occurred in the first 10 s of ischemia, after which contractile function transiently stabilized and then fell at a slower rate. During reperfusion, recovery of relaxation was impaired relative to recovery of contractile function. A second period of ischemia and reflow produced changes in contractility, relaxation, and lactate production virtually identical to the initial one. In the absence of glycolytic blockade, tissue lactate accumulation developed, no contracture occurred, the pacing threshold did not increase, and reperfusion after 3 min of ischemia resulted in complete recovery of contractile function. Glycolytic blockade with 0.1 mM iodoacetate (IAA) prevented ischemic lactate production, accelerated the fall in contractility, caused irreversible contracture after 30 s of ischemia, an irreversible increase in pacing threshold within 3 min of ischemia, and poor recovery of contractile function with reperfusion. Thus during the first 3 min of severe ischemia, glycolysis exerted a net beneficial effect on myocardial function despite significant tissue lactate accumulation.

Animals↗
PubMed1978

Renin-angiotensin system inhibition in conscious sodium-depleted dogs. Effects on systemic and coronary hemodynamics.

The role of the renin-angiotensin system in the regulation of the systemic and coronary circulations during sodium depletion was studied in conscious normotensive dogs by i.v. administration of teprotide (0.5 mg/kg), an angiotensin-converting enzyme inhibitor, and saralasin (0.05-5 mug/kg per min), an angiotensin-receptor antagonist. Sodium depletion was produced by administering a low sodium diet and furosemide for 5 days. Administration of both teprotide and saralasin lowered systemic arterial blood pressure and total peripheral vascular resistance. Simultaneously, cardiac output increased, but left ventricular end-diastolic pressure, dP/dt, and dP/dt/P did not change significantly. Furthermore, both agents reduced diastolic coronary vascular resistance and increased coronary blood flow, but did not affect myocardial oxygen consumption, left ventricular work, or myocardial efficiency. These systemic and coronary vasodilator effects of teprotide and saralasin, however, were not observed in normal dogs on a regular sodium diet; in this group, the only effect noted was a slight increase in arterial pressure during saralasin infusion. Arterial plasma concentration of norepinephrine did not differ between normal and sodiumdepleted dogs, nor did it change significantly after teprotide administration. These results suggest that, during salt depletion, angiotensin II exerts an active vasoconstrictor action on the systemic and coronary vessels, but has no significant effects on myocardial contractility or energetics. It also appears likely that the increase in cardiac output observed in sodiumdepleted dogs after angiotensin inhibition was caused, at least in part, by the decrease in systemic arterial pressure.

Angiotensins↗
PubMed1978

ST-segment elevation during recovery from exercise. A new manifestation of Prinzmetal's variant angina.

Four patients underwent exercise testing because of a history of pain in the chest; all four developed marked elevation of the S-T segment only during recovery after exercise. Three of the four patients showed ST-segment depression during exercise, but ST-segment elevation was absent until two or more minutes after cessation of exercise. ST-segment elevation after exercise was accompanied by hypotension in three patients and by ventricular arrhythmias in one. Subsequent coronary angiographic studies revealed normal or minimally diseased coronary arteries in two patients and significant coronary lesions in the other two. Review of the literature shows that contrary to the prevailing belief, over half of the patients with Prinzmetal's variant angina have electrocardiographic changes diagnostic of ischemia during exercise testing. Over half of the patients with abnormal findings on tests during exercise display ST-segment elevation as a manifestation of ischemia; however, delayed ST-segment elevation of the type seen in these four patients is distinctly uncommon, having previously been described in only three individual case reports. The pathophysiology of this response is uncertain but may relate to rapid alterations in the autonomic balance during recovery after exercise.

Adult↗
PubMed1978

Experimental myocardial infarction. 14. Accelerated myocardial stiffening related to coronary reperfusion following ischemia.

In six dogs with surgically opened chests, segmental mechanical function was determined by measuring segment length using mercury-in-Silastic gauges attached to the epicardial surface of the left ventricular wall. Following coronary arterial occlusion the amplitude of the resulting paradoxical systolic bulge was quantitated in terms of "muscle lengths", defined as the ratio of the amplitude of the segment length over the end-diastolic segment length (EDSL). From an excursion of 0.176 +/- 0.029 muscle lengths at six hours of ischemia, the amplitude of the bulge decreased abruptly to 0.125 +/- 0.024 muscle lengths after 15 minutes of coronary reperfusion (P less than 0.05) but maintained paradoxical expansion in systole. Segmental "effective stiffness", calculated at the same periods of time from end-diastolic pressure-length relationships during transient pressure loading of the left ventricle, showed a reciprocal change, increasing from 1.416 +/- 0.161 to 2.051 +/- 0.238 mm Hg/% deltaEDSL (P less than 0.05). These data indicate that the degree of paradoxical bulging of an ischemic segment is affected by its pressure-length characteristics (distensibility) and that a rapid decrease both in the amplitude of the bulge and in distensibility occurs during reperfusion. The mechanism is uncertain but may relate to either myocardial edema or myofibrillar contracture.

Animals↗
PubMed1978

Ambulance utilization by patients with acute myocardial infarction.

Fifty-five per cent (73/133) of myocardial infarction (MI) patients on Cape Cod during a three-month period reached the hospital by ambulance. the 45 per cent (60/133) not using ambulances were compared to users to identify a subpopulation to which public health programs might be directed to increase appropriate use of cardiac ambulances. Univariate analyses showed a distnce of more than ten miles from the hospital, and a prior history of MI distinguished ambulance users from non-users. Demographic/economic status, delay in seeking care, presenting symptoms, Killip class, and in-hospital mortality rates were not signigicantly different. Step-wise discriminant analysis identified four predictive variables in rank order: distance from the hospital, past history of MI, symptoms of fainting, and negative history for hypertension which correctly classified 72 per cent of our population with respect to ambulance utilization.

Aged↗
PubMed1977

Bayesian analysis of electrocardiographic exercise stress testing.

We evaluated the diagnostic accuracy of exercise-induced ST-segment depression in detecting coronary-artery disease by applying the likelihood-ratio formulation of Bayes's theorem to stress-test data, which were partitioned into half-millimeter ranges of depression. The graphic relation between the predictive value of a given test result and the pretest risk of disease in the test subjects was obtained for each of these half-millimeter intervals. This method reveals that the predictive value of testing depends on the degree of ST-segment depression, and that the pretest risk of coronary-artery disease is an important determinant of the predictive value of any test result in the individual patient. These findings suggest that the use of the terms "positive" and "negative" are inappropriate to describe most stress-test results. Instead, the results should be interpreted in terms of a continuum of risk based on the extent of ST-segment depression.

Adult↗
PubMed1977

Symptomatic myocardial infarction without chest pain: prevalence and clinical course.

Symptomatic myocardial infarction without chest pain was identified in 26 of 102 patients (25.5%) admitted to the hospital with acute myocardial infarction. As a group, these patients had a significantly lesser prevalence of a history of angina (P less than 0.05) and cigarette smoking (P less than 0.01). Their mean age was 69.1 years compared with 58.7 years for patients with chest pain (P less than 0.001). The group had a significantly greater median delay between the onset of symptoms and (1) arrival at the hospital (P less than 0.05), (2) examination by a physician in the emergency room (P less than 0.05), (3) diagnosis of possible myocardial infarction (P less than 0.001), and (4) transfer from the emergency room to the intensive care unit (P less than 0.001). They had significantly higher admission values for mean heart rate, respiratory rate, temperature and white blood cell count and more frequent in-hospital complications of pneumonia (P less than 0.001) and cardiogenic shock (P less than 0.05). Mortality in the group was 50% compared with 18% in the group with chest pain (P less than 0.05). Discriminant function analysis identified an at-risk population with 80% reliability.

Abdomen↗
PubMed1977

Precordial ST-segment mapping 3. Stability of maps in the early phase of acute myocardial infarction.

To evaluate the stability of precordial ST-segment mapping techniques in assessing ischemic myocardial injury, we studied 28 patients with acute anterior myocardial infarction using a 49-lead electrocardiographic system (1 mV. = 10 mm.). The sum of ST elevations in millimeters was taken as an index of ischemic injury, and remained stable in two consecutive maps made approximately one hour apart (65.8 +/- 8.4 vs. 63.8 +/- 8.7 mm.). The number of sites showing ST elevation larger than or equal to one mm. was taken as an index of extent of injury, and showed a small but statistically significant decline (23.9 +/- 4.5 vs. 22.3 +/- 4.2 mm.) during the same time interval. Blood pressure and heart rate remained stable. Changes in the map were observed in five patients, but could be explained in four by abrupt alterations in clinical status. In one patient no explanation for alterations in the map was apparent. We conclude that precordial ST segment maps are usually stable in the early stages of anterior myocardial infarction, but should be used to evaluate interventions only with careful clinical monitoring, and with the knowledge that occasional unexplained variations do occur.

Acute Disease↗
PubMed1977

Regulation of cardiac output during 2,4-dinitrophenol-induced tissue hypermetabolism in the dog.

1. Cardiac output increased in proportion to oxygen consumption in intact chloralose-anaesthetized dogs after four successive intravenous infusions of 2,4-dinitrophenol (11 mumol/kg; 2 mg/kg). 2. Splenectomy abolished the increase in cardiac output after the first three doses of 2,4-dinitrophenol. beta-Adrenoreceptor blockade by practolol, on the other hand, did not prevent the cardiac output rise after the first 2,4-dinitrophenol infusion, but further increases by 2,4-dinitrophenol infusion were abolished. When splenectomy and beta-adrenoreceptor blockade were combined, cardiac output did not increase significantly after all four doses of 2,4-dinitrophenol. 3. Cardiac output and mean systemic arterial blood pressure increased when the splenic venous blood collected after 2,4-dinitrophenol infusion was infused intraportally. 4. In a vascularly isolated, but normally innervated, lower half-body cross-perfusion preparation, cardiac output and mean systemic arterial blood pressure increased in the upper half-body when tissue hypermetabolism was produced in the cross-perfused area by 2,4-dinitrophenol. Neith pulmonary artery wedge pressure nor heart rate changed significantly. 5. This circulatory stimulation, after regional 2,4-dinitrophenol infusion, was abolished or was prevented from occurring by splenectomy. 6. It appears that the normal cardiac output response to tissue hypermetabolism requires both an intact spleen and normally functioning beta-adrenoreceptors.

Animals↗