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Biomedical subjects

T C Smitherman

Publications and source records attributed to T C Smitherman.

At least 37 records · Page 2Linked to original sources
PubMed1981

Echocardiography in unstable angina.

This study was undertaken to determine whether abnormalities on the echocardiograms of patients with unstable angina have any prognostic significance. 27 male patients, mean age 53 years, who fulfilled criteria for unstable angina and who responded to medical therapy, had echocardiograms within 48 h of admission and at discharge. Follow-up data were obtained from 7 patients during a postdischarge period of 6-26 weeks. 13 patients had mild exertional angina or were pain-free (group I) and 14 patients had either severe, stable angina pectoris or recurrence of their unstable angina (group II) during the follow-up period. When admission and discharge values were compared, the echocardiographic ratio of left ventricular end-diastolic dimension to mitral valve closure time (EDD/PR-AC) showed significant differences for both group I and group II (p less than 0.05). An abnormal EED/PR-AC ratio was present at discharge in 8 of 14 group II patients compared to only 1 of 13 group I patients (p less than 0.05). The mean values for end-diastolic dimension, mitral valve closure time, and amplitudes of interventricular septal and posterior left ventricular wall motion were not significantly different in comparisons between admission and discharge studies and between group I and group II patients. In 19 patients who had cardiac catheterization druing the follow-up period, the discharge EED/PR-AC ratio correlated inversely with the angiographic ejection fraction (r = 0.79; p less than 0.001).

Adult↗
PubMed1980

Submaximal exercise testing after unstable angina.

Sixty-one consecutive men, mean age 56 years, who fulfilled criteria for unstable angina and who responded to medical therapy, underwent submaximal exercise testing prior to hospital discharge and at least 3 days after their last episode of angina. Forty-two patients were receiving propranolol at the time of exercise. Submaximal exercise was targeted to 120 beats/minute and strict criteria for the premature termination of each study were followed. Follow-up data were available on 55 patients post-discharge over a period of 6 to 36 weeks. No patient suffered recurrence of unstable angina or myocardial infarction due to the exercise test. Exercise was prematurely terminated by an ischemic response (chest pain and/or ST segment changes) in 34 patients (56%) and by leg fatigue in 13 patients (21%). Only five patients had exercise-induced ventricular ectopic activity, four of whom were not receiving propranolol. Nine patients achieved the target heart rate. Exercise-induced abnormal electrocardiographic changes predicted the postdischarge recurrence of episodes of unstable angina (p less than 0.05). Comparison of predischarge submaximal exercise data with postdischarge maximal exercise shows that recovery in cardiovascular function after unstable angina occurs soon after stabilization and prior to the submaximal test.

Adult↗
PubMed1980

Estimation of myocardial involvement in patients with acute myocardial infarction by two-dimensional echocardiography.

To determine whether real-time two-dimensional echocardiography (2-D echo) can estimate the extent of myocardial involvement in patients with acute myocardial infarction (MI), regional wall motion on serial short-axis 2-D echo recordings was analyzed and the summed scores were compared with estimates of infarct involvement by thallium-201 reperfusion (Tl) and technetium-99m stannous pyrophosphate (99mTc-PYP) scintigraphy. Thirty-two consecutive male patients admitted with their first MI were studied; 10 patients had anterior, 16 had inferior and six had subendocardial MIs. Two patients were technically unsuitable for 2-D echo studies. Twenty patients had Tl scintigrams and 29 had 99MTc-PYP scintigrams. Summed 2-D echo scores correlated closely with estimates of infarct involvement by Tl (r = 0.87) and with estimates of infarct size by 99mTc-PYP (r = 0.74). The location of MI by 2-D echo agreed with the electrocardiographic location in 26 of 29 patients; discrepancies occurred in one inferior and two subendocardial MIs. Predischarge 2-D echo failed to identify extension of transmural infarction. However, two patients whose subendocardial MIs progressed to transmural MIs were identified. This study shows that 2-D echo is a valid method for the early estimation of the extent of myocardial involvement in patients with acute MI, especially transmural MIs. In particular, 2-D echo correlates closely with Tl reperfusion scintigraphy because both detect areas of ischemia and infarction.

Adult↗
PubMed1980

Studies on human heart citrate synthase.

Citrate synthase from human heart was purified by affinity chromatography with Sepharose-ATP. The molecular weight (100,000) and the presence of two presumably identical subunits do not differ from other mammalian citrate synthases. However, the kinetics constants and immunologic characteristics of the enzyme differed from other mammalian citrate synthases. The Km values for acetyl-CoA (0.4 microM) and oxaloacetate (0.25 microM) were about an order of magnitude lower than those previously found for other mammalian (and eucaryotic) citrate synthases. The kinetics constants for the reverse reaction Km for citrate (420 microM) and CoA (70 microM), were of similar magnitude to the values for other mammals. Anti-human heart antiserum developed a single precipitin line in an Ouchterlony plate against a heart extract, no precipitin line with brain, and a precipitin line with spurs against liver and kidney extract. Following myocardial infarction in men, the enzyme appeared in peripheral blood rarely and in low concentration in contrast with earlier experiences with experimental infarction in dogs.

Animals↗
PubMed1979

Detection of myocardial infarct extension by CK-B radioimmunoassay.

Myocardial infarct extension after the acute event was defined as a second reise in the myocardial isoenzyme of serum creatine kinase (CK-B) after the initial return of CK-B to normal values. In 43 patients with acute myocardial infarcts, CK-B was measured by radioimmunoassay every 12 hours for 14 days. Nineteen patients had anterior transmural myocardial infarcts AMI, 14 had inferior transmural myocardial infarcts (IMI) and 10 had subendocardial myocardial infarcts (SEMI). Infarct extension as detectd by a second rise in serum CK-B occurred in six patients (32%) with AMI, two (14%) with IMI and two (20%) with SEMI; these differences are not statistically significant. Infarct extension for all patients combined was 23%. Four patients with AMI also had infarct extension as determined by recurrent chest pain. ECG alterations and other enzyme changes. In the other six, the infarct extension was undetected clinically. Four patients with AMI and infarct extension died within 3 weeks after hospitalization. We did not note any additional morbidity or mortality in patients with infarct extension who had IMI or SEMI. There was no significant difference in the frequency of previous myocardial infarction, history of hypertension, diabetes mellitus or smoking history in patients with and without infarct extension shown by serum CK-B isoenzyme elevations. The measurement of serum CK-B values with a quantitative and sensitive assay suggests that myocardial infarct extension occurs more commonly than clinically recognized, but the frequency of extension may be less than that reported in patients in whom precordial mapping and total serum CK values were measured to identify this phenomenon.

Adult↗
PubMed1979

Myocardial contractility in patients with ischemic heart disease during long-term administration of quinidine and procainamide. Direct measurement of segmental shortening with radiopaque epicardial markers.

The purpose of this investigation was to determine whether long-term oral administration of commonly prescribed doses of quinidine sulfate and procainamide hydrochloride to patients with ischemic heart disease affects myocardial contractility. Segmental contractility, assessed by the systolic shortening fraction, the relative change in interclip distance from diastole to systole, was measured by cineradiography of metal clips that had been sutured to the epicardium at the time of coronary artery bypass surgery. Global contractility was assessed by gated blood-pool scintigraphy. Systolic shortening fraction determinations and scintigraphy were obtained following five to seven days' administration of procainamide (500 mg every four hours), quinidine (200 mg every six hours), or neither drug in a random sequence. Serum drug levels (milligrams per liter) were 1.8 +/- 0.8 (mean +/- 1 SD) for quinidine and 3.7 +/- 1.1 for procainamide, when measured one hour before the next dose. During quinidine administration, mean segment shortening fraction decreased only slightly, but significantly (P less than 0.02), from 12.4 percent to 10.6 percent. The clinical importance of so small a change is questionable. During procainamide administration, there was a very small, insignificant (P greater than 0.9), decrease in segmental shortening. Global left ventricular function was not significantly changed by either drug. It appears that both drugs can be used over long periods in commonly prescribed doses in patients with ischemic heart disease without a major overall deleterious effect on cardiac performance.

Blood Pressure↗
PubMed1977

Influence of mannitol on contractile responses of isolated perfused arteries.

The influence of hyperosmotic mannitol on vascular smooth muscle contractile responses was examined in isolated arterial preparations. Vasoconstrictor effects of norepinephrine (NE) and potassium chloride (K+) in the perfused central artery of the rabbit's ear and in perfused mesenteric arteries of cats were significantly inhibited by infusion with Krebs bicarbonate solution made hyperosmotic with mannitol (50-200 mosM increase). Similarly, the magnitude and duration of vasoconstrictor responses to transmural stimulation of the central ear artery of the rabbit were decreased by hyperosmotic mannitol (50 mosM). Mannitol (50 mosM) produced a decrease in perfusion pressure when perfusion pressure was maintained at an increased level by K+ (60 mM). Mannitol-induced vasodilatation was not affected by ethacrynic acid (1.5 X 10(-5) M), beta adrenergic blockade or by the development of tachyphylaxis to the vasodilator effects of nitroglycerin. The concentration of cyclic adenosine-monophosphate was not changed by mannitol. Isotonic mannitol also inhibited NE-induced contractile responses. These data indicate that hyperosmotic mannitol produces vasodilatation in isolated arterial smooth muscle by a mechanism(s) that appears dissimilar from that of several other vasodilator substances and suggest that hypertonicity may not be the only factor involved in the vasodilator effect of mannitol.

Animals↗
PubMed1975

Pulmonary atresia with ventricular septal defect: report of the oldest known surviving case.

The case of a 54-year-old housewife, oldest published survivor with pulmonary atresia and a ventricular septal defect (pseudotruncus arteriosus), is reported. Her remarkably favorable course is likely related to the absence of progressive hemodynamic changes, with moderate pulmonary flow adequate for nearly normal arterial oxygenation yet without increasing pulmonary vascular resistance. This case reemphasizes the relationship of longevity to pulmonary blood flow volume with this defect.

Cardiomegaly↗