Search PubMed⌕ Search

Biomedical subjects

R Roberts

Publications and source records attributed to R Roberts.

At least 559 records · Page 31Linked to original sources
PubMed1979

Abnormal technetium-99m pyrophosphate images in unstable angina: ischemia versus infarction?

There is controversy concerning the specificity of myocardial infarct imaging with technetium-99m pyrophosphate due to the high frequency of false positive images, especially in patients with unstable angina. In this study technetium-99m pyrophosphate images were compared with frequent determinations of plasma creatine kinase, MB isoenzyme (MB CK) activity in 116 patients admitted with the diagnosis of unstable angina. It was hypothesized that frequent measurement of MB CK activity, a sensitive and specific marker for myocardial necrosis, using sensitive assay techniques would detect small amounts of myocardial necrosis which might have been unrecognized by conventional clinical methods. The scintigraphic results and isoenzyme determinations agreed in 88 percent of patients; both tests were normal in 69 percent and both were abnormal, indicating acute myocardial infarcation, in 19 percent of patients. In the remaining 14 patients (12 percent), the scans were abnormal, but MB CK activity was normal. In five of these patients (4 percent), abnormal scintigrams presumably reflected persistent scan positivity after previous myocardial infarction. Only the remaining nine patients (8 percent) could be classified as having unexplained false positive scans, a frequency substantially less than that reported by other investigators who based the diagnosis of myocardial infarction on conventional clinical criteria. These results suggest that abnormal technetium-99m pyrophosphate images in patients with unstable angina generally indicate myocardial necrosis.

Adult↗
PubMed1979

Reduction of early ventricular arrhythmia by acebutolol in patients with acute myocardial infarction.

To assess the effects of intravenously administered acebutolol (1-20 mg every 4 hours for 24 hours) on cardiac rhythm and performance, we studied 72 patients with evolving myocardial infarction. Twenty-five patients were treated with acebutolol beginning 6 hours after the first increase in the level of plasma creatine kinase. Enzymatically estimated infarct size was compared with that of 25 controls matched for predicted infarct size. Observed infarct sizes were not significantly different in the 2 groups (37 +/- 5 and 30 +/- 5 CK-gram equivalents, respectively). Mean heart rate, diastolic blood pressure, and cardiac output declined from control values during treatment with acebutolol, but remained within the normal range. Mean pulmonary artery pressure and pulmonary artery occlusive pressure were unchanged. In a group of 22 treated patients matched with 22 control subjects for frequency of ventricular extrasystoles, acebutolol effected a prompt reduction in frequencies of ventricular extrasystoles and repetitive arrhythmias, whereas values were not significantly changed in controls during the corresponding intervals. Accordingly, acebutolol may be a useful antiarrhythmic agent in selected patients with acute myocardial infarction with adversely altering haemodynamic stability or enzymatically estimated infarct size.

Acebutolol↗
PubMed1979

The Admirable H.

Explore the source record for details and available documents.

Australia↗
PubMed1979

Four tribes.

Explore the source record for details and available documents.

Australia↗
PubMed1978

Studies on the pharmacokinetics and pharmacodynamics of atenolol in man.

The non-stimulant cardioselective beta adrenocepter antagonist atenolol has been studied in volunteers in order to define its pharmacokinetic characteristics. Atenolol (100 and 200 mg orally) is rapidly absorbed, reductions in heart rate and systolic pressure being observed in 30 min. The effect persists for up to 8 h. Over 85% of an intravenous dose is excreted in urine within 24 h but only 50% of an oral dose. The bioavailability of approximately 50% is due to reduced absorption. Peak blood levels are observed at 2-4 h and the half life of atenolol given orally is 5-6 h. Atenolol reduces the cardiac response to standing and head-up tilt. It does not reduce circulating levels of renin but slightly impairs the renin response to tilt. Atenolol both orally and intravenously reduces supine diastolic pressure about four hours after administration, the effect persisting for up to 24 h.

Administration, Oral↗
PubMed1978

Progressive nature of myocardial injury in selected patients with cardiogenic shock.

To determine whether the extensive myocardial injury associated with cardiogenic shock in some patients results from a progressive rather than a discrete massive insult, a study was made of 15 selected patients who had cardiogenic shock within 48 hours of admission, 5 patients with hypovolemic shock without myocardial infarction and 11 patients with myocardial infarction without shock. Peak plasma MB creatine kinase (CK) activity was significantly higher in the seven patients with cardiogenic shock associated with initial infarction (213 international units [IU]/liter) than in patients with shock and previous infarction (98 IU/liter) and in patients with uncomplicated myocardial infarction (125 IU/liter). A prolonged time to peak MB CK activity (averaging 26 hours) and a plateau of elevated MB CK activity were seen in patients with shock associated with initial infarction. Because shock itself did not slow the rate of apparent MB CK disappearance, results obtained suggest that cardiogenic shock associated with initial infarction in selected patients results from progressive myocardial damage underlying continuing release of MB CK into the circulation. The findings are compatible with the concept that, in these patients, cardiogenic shock reflects a vicious cycle of spreading myocardial injury, progressive compromise of cardiac function, exacerbation of ischemia and perpetuation of myocardial damage.

Creatine Kinase↗
PubMed1978

99mTc-pyrophosphate imaging in acute pericarditis: a clinical and experimental study.

Fifteen patients with clinical and electrocardiographic features of acute pericarditis underwent myocardial scintigraphy using 99mTc-pyrophosphate. All had normal images. In 5 additional patients with acute pericarditis and evidence of ischemic heart disease, 99mTc-pyrophosphate images showed focal abnormalities in 2 patients and equivocal findings in 2. Serial myocardial radionuclide images were obtained 2 to 18 days after induction of pericarditis in 8 dogs; all images were normal. No stainable tissue calcium was demonstrated histochemically in the pericardium or myocardium of these dogs. Our results suggest that 99mTc-PYP myocardial radionuclide images are normal in acute pericarditis in the absence of ischemic heart disease.

Acute Disease↗