Myocardial Oxygen Demand (myocardial + oxygen_demand)

Distribution by Scientific Domains

Selected Abstracts

The effect of diabetes on heart rate and other determinants of myocardial oxygen demand in acute coronary syndromes

K. Foo
Abstract Aims To compare major determinants of myocardial oxygen demand (heart rate, blood pressure and rate pressure product) in patients with and without diabetes admitted with acute coronary syndromes. Methods A cross-sectional study of the relation between diabetes and haemodynamic indices of myocardial oxygen demand in 2542 patients with acute coronary syndromes, of whom 1041 (41.0%) had acute myocardial infarction and 1501 (59.0%) unstable angina. Results Of the 2542 patients, 701 (27.6%) had diabetes. Major haemodynamic determinants of myocardial oxygen demand were higher in patients with than without diabetes: heart rate 80.0 ± 20.4 vs. 75.2 ± 19.2 beats/minute (P < 0.0001); systolic blood pressure 147.3 ± 30.3 vs. 143.2 ± 28.5 mmHg (P = 0.002); rate-pressure product 11533 ± 4198 vs. 10541 ± 3689 beats/minute × mmHg (P < 0.0001). Multiple regression analysis confirmed diabetes as a significant determinant of presenting heart rate [multiplicative coefficient (MC) 1.05; 95% confidence interval (CI) 1.03,1.07; P < 0.0001], rate pressure product (MC 1.09; CI 1.05,1.12; P < 0.0001) and systolic blood pressure, which was estimated to be 3.9 mmHg higher than in patients without diabetes (P = 0.003). These effects of diabetes were independent of a range of baseline variables including acute left ventricular failure and mode of presentation (unstable angina or myocardial infarction). Conclusions In acute coronary syndromes, heart rarte and other determinants of myocardial oxygen demand are higher in patients with than without diabetes, providing a potential contributory mechanism of exaggerated regional ischaemia in this high-risk group. [source]

Arterial structural and functional alterations in uraemia

A. P. Guérin
Abstract Epidemiological and clinical studies have shown that cardiovascular disease in patients with end-stage renal disease (ESRD) is frequently related to damage of large conduit arteries. Arterial disease is responsible for the high incidence of ischaemic heart disease, peripheral artery diseases, left ventricular hypertrophy and congestive heart failure. The vascular complications in ESRD are ascribed to two different but associated mechanisms, namely atherosclerosis and arteriosclerosis. Whereas the former principally affects the conduit function with ischaemic lesions being the most characteristic consequence, the latter primarily disturbs the dampening function of large arteries. Arteriosclerosis in ESRD patients is characterized by diffuse dilation and wall hypertrophy of large conduit arteries and stiffening of arterial walls. These changes represent a clinical form of an accelerated ageing process. The main clinical characteristics due to arterial stiffening are isolated increase in systolic blood pressure with normal or lower diastolic pressure resulting in an increased pulse pressure. The consequences of these alterations are: (i) an increased left ventricular afterload with development of left ventricular hypertrophy and increased myocardial oxygen demand; and (ii) altered coronary perfusion and subendocardial blood flow distribution. Epidemiological studies have identified arterial remodelling and stiffening as independent predictors of overall and cardiac mortality in ESRD patients. [source]

Heart rate variability , a therapeutic target?

H. C. Routledge
Reduced heart rate variability (HRV) is a powerful and independent predictor of an adverse prognosis in patients with heart disease and in the general population. The HRV is largely determined by vagally mediated beat to beat variability, conventionally known as respiratory sinus arrhythmia. Thus, HRV is primarily an indicator of cardiac vagal control. It is still unclear whether the relationship between measures of cardiac vagal control and mortality is causative or mere association. Possible mechanisms by which cardiac vagal activity might beneficially influence prognosis include a decrease in myocardial oxygen demand, a reduction in sympathetic activity and a decreased susceptibility of the ventricular myocardium to lethal arrhythmia. In animals, augmentation of cardiac vagal control by nerve stimulation or by drugs is associated with a reduction in sudden death in susceptible models. In humans a number of drugs which have been shown to reduce mortality and sudden death in large randomised trials can also be demonstrated to increase HRV. As a result of this evidence, it has been suggested that the effect of drugs or other therapeutic manoeuvres on HRV might be used to predict clinical efficacy. The use of HRV as a therapeutic target is discussed in this review. [source]

Effects of levosimendan on indocyanine green plasma disappearance rate and the gastric mucosal,arterial pCO2 gradient in abdominal aortic aneurysm surgery

Background: Levosimendan has a dual mechanism of action: it improves myocardial contractility and causes vasodilatation without increasing myocardial oxygen demand. In a laboratory setting, it selectively increases gastric mucosal oxygenation in particular and splanchnic perfusion in general. The aim of our study was to describe the effects of levosimendan on systemic and splanchnic circulation during and after abdominal aortic surgery. Methods: Twenty abdominal aortic aneurysm surgery patients were randomized to receive either levosimendan (n=10) or placebo (n=10) in a double-blinded manner. Both the mode of anaesthesia and the surgical procedures were performed according to the local guidelines. Automatic gas tonometry was used to measure the gastric mucosal partial pressure of carbon dioxide. Systemic indocyanine green clearance plasma disappearance rate (ICG-PDR) was used to estimate the total splanchnic blood flow. Results: The immediate post-operative recovery was uneventful in the two groups with a comparable, overnight length of stay in the intensive care unit. Cumulative doses of additional vasoactive drugs were comparable between the groups, with a tendency towards a higher cumulative dose of noradrenaline in the levosimendan group. After aortic clamping, the cardiac index was higher [4(3.8,4.7) l/min/m2 vs. 2.6(2.3,3.6) l/min/m2; P<0.05] and the gastric mucosal,arterial pCO2 gradient was lower in levosimendan-treated patients [0.9(0.6,1.2) kPa vs. 1.7(1.2,2.1) kPa; (P<0.05)]. However, the total splanchnic blood flow, estimated by ICG-PDR, was comparable [29(21,29)% vs. 20(19,25)%; NS]. Organ dysfunction scores (sequential organ dysfunction assessment) were similar between the groups on the fifth post-operative day. Conclusion: Levosimendan favours gastric perfusion but appears not to have a major effect on total splanchnic perfusion in patients undergoing an elective aortic aneurysm operation. [source]

Effects of moderate acute isovolaemic haemodilution on myocardial function in patients undergoing coronary surgery under volatile inhalational anaesthesia

ANAESTHESIA, Issue 3 2009
S. G. De Hert
Summary When myocardial oxygen demand is increased by elevated heart rate in patients undergoing coronary artery surgery under total intravenous anaesthesia, acute isovolaemic haemodilution may be associated with a deterioration of cardiac function. We investigated the effects of acute isovolaemic haemodilution during volatile inhalational anaesthesia. Forty patients undergoing coronary surgery were randomly assigned to two groups according to the rate of atrioventricular pacing (Group 70 at 70.min,1 and Group 90 at 90.min,1). While paced at the fixed heart rate, acute isovolaemic haemodilution was performed before the start of cardiopulmonary bypass. In both groups mean (SD) stroke volume increased with haemodilution (from 65 (9) to 83 (10) ml.min,1 (p < 0.01) in Group 70 and from 65 (9) to 81 (9) ml.min,1 (p < 0.01) in Group 90) as a result of a decrease in systemic vascular resistance (from 1175 (231) to 869 (164),5 (p < 0.01) and from 1060 (185) to 849 (146),5 (p < 0.01), respectively) and an increase in end-diastolic volume (from 1049 (234) to 1405 (211) ml (p < 0.01) and from 1078 (106) to 1438 (246) ml (p < 0.01), respectively). Left ventricular pressure-derived data remained unchanged with acute isovolaemic haemodilution in both groups. [source]

Cocaine and Ethanol: Combined Effects on Coronary Artery Blood Flow and Myocardial Function in Dogs

Lance D. Wilson MD
Abstract Objectives:, In combination, cocaine and ethanol are more cardiotoxic than is either substance alone. These substances together constitute a drug abuse combination that commonly results in fatality. Previously the authors have demonstrated that cardiotoxicity of cocaine and ethanol is in part due to synergistic myocardial-depressant effects. However, it remains unclear whether this myocardial depression is associated with concomitant adverse effects on coronary blood flow in relation to these substances. The aim of this study was to investigate combined effects of cocaine and ethanol on myocardial blood flow, in relation to indices of myocardial function. Methods:, Anesthetized dogs were instrumented for hemodynamic monitoring with Doppler flow probes placed on the circumflex and left anterior descending (LAD) coronary arteries. Dogs were randomized to three groups (each n = 6): ethanol (E, 1.5 g/kg followed by placebo), cocaine (C, placebo followed by cocaine, 7.5 mg/kg IV), or cocaine plus ethanol (C + E). All measurements were made at control, after placebo or ethanol, and then at fixed time intervals after cocaine or placebo bolus over 3 hours. Results:, In both the C + E and the C groups, circumflex blood flow (CBF) decreased by 71% (95% confidence interval [CI] = 56% to 85%) and 57% (95% CI = 43% to 72%, both p < 0.04 vs. baseline) immediately after cocaine bolus. This was associated with transient depression of cardiac output, myocardial contractile function, and rate-pressure product (RPP), all indices of myocardial oxygen demand. A subsequent rebound increase of coronary sinus blood flow (CSBF) of 56% (95% CI = 26% to 137%, p < 0.03) compared to baseline occurred only in the C group and was associated with increases of myocardial contractile function and RPP. In the C + E group, 2 hours after drug administration, there was a decrease in CSBF of 49% (95% CI = 32% to 67%; p < 0.01) compared to baseline, which was associated with concomitant numerical decreases of the indices of myocardial oxygen demand and accumulation of cocaethylene. Conclusions:, Acute decreases in myocardial flow secondary to cocaine, and cocaine and ethanol in combination, were similar and temporally associated with cocaine's direct myocardial-depressant effects. Rebound increases in myocardial function and blood flow due to cocaine were attenuated by ethanol. Delayed myocardial depression and decreases in myocardial blood flow were observed only with coadministration of cocaine and ethanol. [source]