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- Cardiovascular Journal of Africa
- OA African Journal Archive
- Volume 9, Issue 1, 1998
Cardiovascular Journal of Africa - Volume 9, Issue 1, 1998
Volumes & issues
Volume 9, Issue 1, 1998
Source: Cardiovascular Journal of Africa 9, pp 10 –12 (1998)More Less
In order to determine if genetically determined immune response factors could play a role in the pathogenesis of infective endocarditis in black patients, we performed HLA-A and HLA-B typing in 38 patients with this disease and HLA-DR and HLA-DQ typing in 33 and 27 of these individuals, respectively. HLA typing was also carried out in a control group of normal black adults. The HLA typing was done by means of a standard microlymphocytotoxicity test. No difference in HLA-A, HLA-B, HLA-DR and HLA-DQ antigen frequencies between patients and controls were noted. This study did not provide any evidence that genetic factors could contribute to a disposition to infective endocarditis.
Source: Cardiovascular Journal of Africa 9, pp 16 –18 (1998)More Less
The presence of caveolae in many cell types including heart myocytes is well established. It is hypothetised that caveolae may play a role in the storing of excess Ca2+ and may be instrumental in Ca2+ transients during contraction and relaxation' in pathological conditions. Furthermore, the presence of substances in caveolae and in their membranes may imply a role in the importing and exporting of key molecules under physiological and pathological conditions. Secretory activity is also suggested by an electron micrograph of rat heart muscle.
Source: Cardiovascular Journal of Africa 9, pp 20 –23 (1998)More Less
In chronic heart failure there is no single explanation for reduced effort tolerance. Recently, abnormalities of skeletal muscles, which include respiratory muscles, have been descriptionbed in cases of chronic heart failure. The aim of this study was to investigate the effect of clinical severity of heart failure, measured by means of the Boston score, on respiratory muscle performance (strength and endurance). Methods. Using the Boston score, we compared 20 patients with chronic heart failure and low ejection fraction to 20 normal people, measuring maximal inspiratory , mouth pressures (MIPs), maximal expiratory mouth pressures (MEPs) and endurance. Endurance was measured by repeated maximal static contractions of MIP and MEP as well as maximal voluntary ventilation (MVV). Results. Inspiratory strength (MIP 75 ï¿½ 34 cmH20) but not expiratory strength (MEP 116.9 ï¿½ 43.7 cmH20) were reduced in heart failure patients, compared with controls (MIP 96.2 ï¿½ 29.2, MEP 120.4 ï¿½ 31 cmH20). Endurance of inspiratory muscles was significantly reduced (P < 0.007) but not of expiratory muscles (P > 0.25). Clinical severity did not correlate with reduced endurance.
Source: Cardiovascular Journal of Africa 9, pp 25 –31 (1998)More Less
Study objective. To determine the acute haemodynamic response of a single dose co-administration of ibopamine plus prazosin in patients with congestive heart failure. Design. A double-blind, placebo-controlled randomized crossover study followed by a 2-week, open safety evaluation. Setting. Wentworth Hospital, Durban. Patients. 12 patients with congestive heart failure who were in functional class (NYHA) II - III. Interventions. All patients underwent right heart catheterisation. On days 1 and 2 the); received study drug or placebo plus prazosin and underwent haemodynamic recordings for 4 hours. Results. Single-dose (200 mg) ibopamine plus prazosin augmented cardiac output (and index) and an early (0 - 60 minute) phasic response in the pulmonary capillary wedge pressure (PCWP) that did not appear to be influenced by the presence of prazosin. The increase in cardiac output was accompanied by a moderate decline in systemic vascular resistance (P = NS) without a change in heart rate. In the open evaluation, 8/14 patients reported adverse events. Six events were considered to be related to study medication of which one (dizziness) occurred in the haemodynamic phase. Conclusion. This study shows that ibopamine has beneficial haemodynamic effects in patients with moderate to severe heart failure. The increase in cardiac output was mild and sustained but with little change in systemic vascular resistance. The early rise in PCWP is not mediated by the a-agonistic vasoconstrictor effects of ibopamine.
Effects of adrenaline, administered early or later after ischaemia, and reperfusion on the isolated rat heartSource: Cardiovascular Journal of Africa 9, pp 35 –39 (1998)More Less
Objective. To evaluate the effect of adrenaline on cardiac function when given early or later in the reperfusion period. Design. Prospective study. Setting. University laboratory. Participants. Wistar rats. Interventions. Isolated rat hearts were subjected to 45 minutes of normothermic ischaemic arrest. During reperfusion, adrenaline was administered early (2 minutes) or later (12 minutes) after termination of ischaemic arrest in addition to a short (S minutes) or longer (10 minutes) recovery period before function was resumed. Measurements and results. Aortic and coronary flow, peak systolic pressure and heart rate were determined before arrest, 10 and 15 minutes after termination of ischaemic arrest. Adenosine triphosphate and creatine phosphate levels were also determined after cardioplegic arrest and reperfusion. Results indicate that early administration of adrenaline was not detrimental but that a longer recovery period after arrest resulted in signiflcantly better cardiac function. Conclusion. After ischaemic arrest of the isolated rat heart a longer recovery period resulted in better cardiac function than a shorter period of recovery.
Source: Cardiovascular Journal of Africa 9, pp 40 –43 (1998)More Less
In order to investigate the flow profiles in the aorta a numerical three-dimensional model of the aortic arch was created. The velocity fields were simulated by applying an inlet velocity corresponding to the physiological velocity of the pressure wave at the aortic valve. The velocity field distribution was found to be uniform throughout the model during the time of increasing inlet velocities. With decreasing inlet velocities a region of low flow developed in the descending portion of the model leading to recirculating flow at the inner wall. At this region of low flow the variation in velocity with time at the inner wall was approximately twice the variation at the outer wall. As a result of the recirculating flow, the wall shear stresses at the inner wall are low and oscillating predisposing to the development of atherosclerosis. This model shows that transient fluid flow in the aortic arch can be simulated. Biological studies are needed to prove that this model can be used to predict sites of pathology.