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Biomedical subjects

M S Ruttley

Publications and source records attributed to M S Ruttley.

At least 37 records · Page 2Linked to original sources
PubMed1989

Post-infarction ventricular septal defect: the importance of right ventricular coronary perfusion in determining surgical outcome.

Mortality from a post-infarction ventricular septal defect (VSD) can be reduced by surgery, selection for which would be helped by knowledge of factors affecting the postoperative prognosis. We reviewed our 9-year experience (1978-1987) of 40 surgically treated patients, comparing preoperative characteristics in those who died postoperatively (n = 15, 37%) and those who survived (n = 25, 63%), all still alive. Sex, age, infarct size as assessed by peak serum creatine kinase values, left ventricular end-diastolic pressure and pulmonary/systemic flow ratio (2.9 +/- 0.2 vs 3.1 +/- 0.3) were similar. Survivors had a lower incidence of inferior infarct than those who died (6, 24% vs 9, 60%, P less than 0.05), a lower incidence of cardiogenic shock (7, 28% vs 10, 67%, P less than 0.05), less elevation of right ventricular end-diastolic pressure (10.1 +/- 0.9 vs 14.7 +/- 1.0 mm Hg, P less than 0.01) and less impairment of right ventricular coronary supply as determined by a coronary angiography-derived myocardial score (0.9 +/- 0.3 vs 4.7 +/- 0.7, P less than 0.001). The data suggest that right ventricular coronary perfusion influences prognosis. The proposed angiographic score may help to identify preoperatively those patients most likely to benefit from surgery.

Cardiac Catheterization↗
PubMed1987

Left main coronary artery occlusion with preserved left ventricular function: a report of three cases.

Three patients with angina pectoris are reported in whom occlusion of the left main coronary artery was found at coronary arteriography. In these three patients left ventricular function was well preserved. In all three the right coronary artery was dominant and there were prominent epicardial and septal collateral vessels to the territories normally supplied by the left anterior descending and circumflex arteries. It seems reasonable to suggest that this coronary artery anatomy and collateral vessel formation accounted for the preservation of the left ventricular myocardium in these patients.

Collateral Circulation↗
PubMed1986

False aneurysm of the femoral artery: computed tomographic and ultrasound appearances.

Twenty-five patients presenting with pulsating masses in the groin, 1-10 days after diagnostic arterial catheterisation, were investigated by computed tomography (CT), ultrasound (US) or both. False aneurysm was demonstrated in 10, four by CT alone, three by US alone and three by both CT and US. Both methods allowed rapid accurate and non-invasive diagnosis of this uncommon complication of arterial catheterisation.

Aneurysm↗
PubMed1986

Computed tomography: the investigation of choice for aortic dissection?

Computed tomography has become established as complementary to aortography in the investigation of patients with suspected aortic dissection. Two cases of dissecting aneurysm are reported in which extensive aortography failed to show evidence of dissection. In both cases dissection was demonstrated by computed tomography. The diagnosis was confirmed in one case at operation and in the other case by follow up. It is suggested that computed tomography is the diagnostic method of first choice in aortic dissection.

Aged↗
PubMed1986

Intracoronary thrombolytic treatment: another hazard.

A patient with acute anterior myocardial infarction was treated with intracoronary thrombolysis. At cardiac catheterisation the first contrast injection into the left coronary artery dislodged some of the thrombus occluding the left anterior descending coronary artery. The thrombus embolised into the circumflex artery where fortunately it fragmented without causing occlusion. The risk of detachment of thrombus should be borne in mind when angiography and thrombolytic treatment are considered in acute myocardial infarction.

Angiography↗
PubMed1985

Pseudocoarctation of the aortic arch associated with bicuspid aortic valve lesion: is it a surgical entity?

Three patients with bicuspid aortic valve lesion associated with pseudocoarctation of the aortic arch are presented. At operation, 2 had a bicuspid calcified stenotic aortic valve, and one a bicuspid non-calcified incompetent aortic valve. All required replacement of the diseased aortic valve. The pseudocoarctation was not corrected because it caused no hemodynamic abnormality.

Adult↗
PubMed1984

The haemodynamic effects of left ventriculography in coronary artery disease and mitral valve disease: a comparison of high and low osmolality contrast media.

We compared the haemodynamic effects of a low osmolality contrast medium Hexabrix 320 (meglumine/sodium ioxaglate) with a high osmolality medium Urografin 370 (meglumine/sodium diatrizoate) in 32 patients. Each underwent left ventriculography with both media, which caused similar small and transient increases in heart rate and systolic pressure. In 15 patients with coronary artery disease, the mean left ventricular end-diastolic pressure increased by 4 mmHg after hexabrix compared with 10 mmHg after urografin (P less than 0.01); it returned to normal more quickly after hexabrix. Changes after both media did not correlate with baseline end-diastolic pressure, ejection fraction, or extent of coronary artery disease, and thus left ventriculography was unhelpful as a stress test. In 14 patients with mitral stenosis, hexabrix produced a smaller increase in left ventricular end-diastolic pressure (P less than 0.001), left atrial pressure (P less than 0.01) and mitral valve gradient (P less than 0.05) than urografin. Patients preferred the low osmolality medium (P less than 0.01). There was no difference in angiographic quality. We advocate low osmolality contrast media for patients with poor left ventricular function or severe mitral stenosis.

Adult↗
PubMed1984

Acute haemodynamic effects of felodipine during beta blockade in patients with coronary artery disease.

The acute effects of felodipine on left ventricular function and haemodynamics were studied in 11 patients with coronary artery disease. To block reflex sympathetic activation due to peripheral vasodilatation and to avoid effects secondary to changes in heart rate all patients received a standard regimen of beta adrenoceptor blockade and all measurements were made during sinus rhythm and right atrial pacing. At 30 minutes after an oral dose (0.075 mg/kg in solution) felodipine plasma concentration were 16.4 (3.5) nmol/l. A significant fall in systemic vascular resistance (30%) and increase in cardiac index (30%) occurred, whereas pulmonary vascular resistance was unchanged. Felodipine increased left ventricular ejection fraction and mean velocity of circumferential fibre shortening but had no effect on derivates of left ventricular pressure (dP/dt or dP/dt P-1) during sinus rhythm or pacing. Thus at the dosage used felodipine was a potent dilator of systemic arterioles but had no direct effect on left ventricular function.

Adult↗
PubMed1981

Acute effects of acebutolol on cardiovascular function in man.

1 The acute cardiovascular effects of acebutolol were measured at constant paced heart rate in thirteen patients investigated for possible coronary artery disease, six of whom showed significant coronary stenosis with regional myocardial dysfunction, seven of whom proved normal. Acebutolol 0.75 mg/kg i.v. was given to three patients with coronary artery disease and three normals, and 1 mg/kg i.v. to the other patients.2 Measurements were made of cardiac output, left ventricular and arterial pressures, and left ventricular angiography. Isovolumic and ejection phase parameters of left ventricular function, and systemic vascular resistance were derived. Plasma levels of acebutolol were measured. 3 The acute effects of acebutolol were a slight fall in cardiac output, LV dp/dt and dP/dt/P. There was no change in LV or arterial pressures, no consistent change in LVEDP or EDV, and no consistent change in ejection fraction or mean VCF. These changes imply a small negative inotropic effect, more marked at the higher dose. 4 The effects of acebutolol differed in patients with ischaemic heart disease compared with normals in that LVEDP and EDV increased, mean VCF decreased and cardiac output was lowered more. 5 These data are consistent with myocardial and vascular effects of beta-adrenoceptor blockade more marked at the higher dose and more marked in patients with ischaemic heart disease.

Acebutolol↗
PubMed1981

Coronary and peripheral arterial responses to ergometrine in patients susceptible to coronary and oesophageal spasm.

Vascular responses to ergometrine were compared in groups of patients subject to coronary artery spasm, or oesophageal spasm, or neither. We measured the degree of diffuse narrowing at different coronary artery sites (not in spasm), and the rise in blood pressure. The data provide no evidence for a generalised sensitivity to alpha-adrenergic stimulation underlying either of these two clinical entities. The left main stem was narrowed significantly less than the three main branches of the coronary artery tree. The degree of diffuse coronary artery narrowing was not influenced by the presence or absence of minor (less than or equal to 50%) fixed stenotic lesions, nor by the initial calibre of the arteries. Ergometrine did not alter arterial lactate concentration or lactate extraction in the absence of coronary spasm.

Adult↗
PubMed1981

Nifedipine and left ventricular function in beta-blocked patients.

We studied the acute effects of nifedipine on left ventricular function and haemodynamics at constant heart rate in patients on beta-blocker therapy. Nifedipine significantly depressed left ventricular peak dP/dt and peak dP/dt x P-1. Nifedipine also significantly reduced systemic vascular resistance: this was associated with decreased systolic blood pressure and increased left ventricular stroke output, with slight non-significant increases of ejection fraction and mean circumferential shortening velocity. There was no change in left ventricular end-diastolic pressure. This clinical study shows that nifedipine increases cardiac output in association with arterial dilatation despite evidence for a negative inotropic effect. Such intrinsic negative inotropic effects would normally be masked by compensatory sympathetic activity.

Atenolol↗
PubMed1977

The electrophysiological evaluation of intravenous acebutolol, a beta-blocking drug.

The electrophysiological effects of acebutolol were studied in 12 patients. Heart rate and systemic arterial pressure were monitored. Plasma acebutolol levels were estimated. The first 6 patients (group A) received 0.3 mg/kg body weight I.V. The subsequent 6 patients (group B) received 0.5 mg/kg body weight I.V. Acebutolol delayed both antegrade and retrograde conduction through the AV node. The effect was greater in group B patients. Effective and functional refractory periods of the AV node were also increased after acebutolol. Intraatrial and intraventricular conduction and the effective refractory periods of the atrium and ventricle were not affected. Acebutolol did not alter significantly the sinus node recovery time or the QTc interval. Heart rate fell, especially where initial rates were fast. Systolic arterial pressure was lowered in group B patients. Peak mean levels of acebutolol were reached 5 min after injection of the drug. In the doses used, acebutolol, although well tolerated, failed to demonstrate electrophysiological evidence of a membrane-stabilizing effect and is therefore unlikely to add to the areas of success achieved by other beta-blocking drugs in the management of arrhythmias.

Acebutolol↗
PubMed1976

A study of the acute electrophysiological and cardiovascular action of disopyramide in man.

The acute electrophysiological and hemodynamic effects of intravenous disopyramide (1.5 mg/kg body weight) were studied in 12 patients with suspected coronary artery disease. Plasma levels of disopyramide were monitored. Disopyramide delayed conduction within the His-Purkinje system and increased the effective refractory period of the atrium. Conduction within the AV node and its refractory period, however, was not significantly altered by the drug. The corrected Q-T interval was significantly increased. Disopyramide increased systemic arterial pressure and slightly raised the left ventricular end diastolic pressure. Heart rate, cardiac and stroke index were unaltered. Peak mean levels of disopyramide were reached 5 minutes after the injection of the drug.

Adult↗