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Objective: There is no obvious explanation, except placebo, to the symptomatic effect of transmyocardial laser revascularization (TMR) in patients with refractory angina. Whether TMR improves myocardial perfusion or relieves symptoms without altering cardiac function is not clarified.Methods: One hundred patients with refractory angina were randomized 1:1 to TMR (CO2 laser) and medical treatment, or medical treatment alone. Technetium 99m (99mTc)-tetrofosmin myocardial perfusion tomography (SPECT), quantitative myocardial perfusion gated SPECT (QGSPECT), technetium 99m (99mTc) multiple gated acquisition radionuclide ventriculografi (MUGA) and cine-magnetic resonance imaging (cine-MRI) were performed at baseline and after 3 and 12 months.Results: Following TMR, a slight reduction in left ventricular ejection fraction (LVEF) (p < 0.05) was observed (MUGA and QGSPECT) compared to baseline. Inclusion of incomplete studies (QGSPECT) revealed a significant reduction in LVEF and increase in left ventricular end-diastolic volume (LVEDV) (p < 0.05) compared to a control group. Otherwise, no between-group comparisons showed statistically significant differences.Conclusion: TMR did not improve myocardial perfusion, but led to a reduction in LVEF and increase in LVEDV, however not significantly different from the control group. [ABSTRACT FROM AUTHOR]

Objectives: The aim of the present study was to examine postoperative serum levels of cardiac enzymes after transmyocardial laser treatment (TML) and to evaluate any associations between this release, postoperative cardiac events and change in ejection fraction after 3 months' follow-up.Design: Forty-nine patients with angina pectoris Canadian Cardiovascular Society Angina Score Class III & IV refractory to medical therapy and untreatable by coronary artery bypass or percutaneous transluminal angioplasty treated with CO2 laser were included. Inclusion criteria were age less than 75 years, left ventricular ejection fraction greater than or equal to 30% and myocardial regions with reversible ischemia. Serum levels of aspartate aminotranspherase (ASAT), alanine aminotranspherase (ALAT) and MB-isoenzymes of creatine kinase (CK-MB) were followed during the first 72 h after surgery. Ejection fractions were estimated by multiple-gated acquisition ventriculography at inclusion and 3 months postoperatively.Results: A significant increase in serum markers of myocardial necrosis was observed 8 h after surgery. A subsequent increase from 8 to 24 h after surgery was associated with the presence of postoperative cardiac adverse events. An inverse correlation was found between peak level of cardiac enzymes and change in ejection fraction from baseline to 3 months' follow-up.Conclusions: TML with CO2 laser is followed by a significant increase in serum levels of cardiac enzymes after 8 h. Further significant increases are associated with cardiac adverse events postoperatively. Peak enzyme values are inversely correlated with change in ejection fraction from baseline to 3 months' follow-up. [ABSTRACT FROM AUTHOR]

Coronary heart disease and beta-blocker treatment can increase the use of the Frank-Starling mechanism during exercise. The aim of the study was to assess whether this could be influenced by physical training. Male patients on beta-blocker treatment after myocardial infarction were randomised to four weeks of training (ET, n = 19) or to a control group (Ctr, n = 18). Cardiac output (CO) at rest and at identical submaximal exercise levels in each patient were determined by radionuclide ventriculography at baseline and after the intervention period. CO was calculated as end diastolic volume (EDV) x ejection fraction x heart rate, and deltaCO and deltaEDV as change in parameter from rest to exercise. The mean (SD) deltaCO decreased from 6.5 (2.1) L/min(-1) to 5.1 (2.4) in ET patients and increased from 5.0 (1.7) to 5.8 (2.7) in Ctr, p = 0.004. deltaEDV decreased from 30 (30) mL to 12 (35) in ET and increased from 11 (20) to 36 (33) in Ctr, p = 0.005. When adjusting for baseline dissimilarities between the groups in a multivariate linear regression analysis, these differences were still statistically significant, p = 0.018 and p = 0.044, respectively. Physical training reduces the CO increase needed to perform identical submaximal exercise, and this is accompanied by less left ventricular dilatation, with a potential for reducing exercise-induced ischaemia. [ABSTRACT FROM AUTHOR]

In an attempt to develop a new approach to the non-invasive measurement of aortic regurgitation, transmitral volumetric flow (MF) and left ventricular total stroke volume (SV) were measured by Doppler and cross sectional echocardiography in 23 patients without aortic valve disease (group A) and in 26 patients with aortic regurgitation (group B). The transmitral volumetric flow was obtained by multiplying the corrected mitral orifice area by the diastolic velocity integral, and the left ventricular total stroke volume was derived by subtracting the left ventricular end systolic volume from the end diastolic volume. The aortic regurgitant fraction (RF) was calculated as: RF = 1 - MF/SV. In group A there was a close agreement between the transmitral volumetric flow and the left ventricular total stroke volume, and the difference between the two measurements did not differ significantly from zero. In group B the left ventricular total stroke volume was significantly larger than the transmitral volumetric flow, and there was good agreement between the regurgitant fractions determined by Doppler echocardiography and radionuclide ventriculography. Discrepancies between the two techniques were found in patients with combined aortic and mitral regurgitation or a low angiographic left ventricular ejection fraction (less than 35%). The effective cardiac output measured by Doppler echocardiography accorded well with that measured by the Fick method. Doppler echocardiography provides a new and promising approach to the non-invasive measurement of aortic regurgitation. [ABSTRACT FROM PUBLISHER]

The effect of intravenous acetazolamide L g on cerebral artery blood velocity and regional blood flow (rCBF) was investigated in eight normal subjects. Blood velocity was measured with 2 MHz pulsed Doppler in the proximal segments of the middle, anterior and posterior cerebral artery (MCA, ACA, and PCA) and in the distal extracranial internal carotid artery (ICA). The rCBF in the regions of interest tentatively corresponding to the perfusion territories of these vessels was estimated usingXe inhalation and a rapidly rotating single photon emission computer tomograph. Both blood velocity and rCBF increased after acetazolamide. There was no significant difference between the percentage ICA blood velocity increase (22 ± 12%) and the percentage rCBF increase in the ICA region of interest (25 ± 9%). In the MCA, ACA, and PCA, however, blood velocity increased more (mean increase 36-42%) than the rCBF in the corresponding regions of interest (mean increase 24-26%). These differences were highly significant suggesting a direct and site specific effect of acetazolamide in narrowing the lumen of the proximal MCA, ACA, and PCA, but not of the extracranial ICA. We also propose that the effect of acetazolamide induces reciprocal changes in the extent of adjacent perfusion territories in individual brain hemispheres. Data compiled from all subjects investigated at two very different perfusion levels (before and after acetazolamide) revealed a significant positive correlation between blood velocity and rCBF. [ABSTRACT FROM AUTHOR]

Cerebral artery blood velocity and regional blood flow (rCBF) were investigated in 17 normal subjects. Blood velocity was measured with 2 MHz pulsed Doppler ultrasound in the proximal segments of the middle, anterior and posterior cerebral artery (MCA, ACA, and PCA) and in the distal extracranial internal carotid artery (ICA). The rCBF in the regions of interest tentatively corresponding to the perfusion territories of these vessels was estimated usingXe inhalation and a rapidly rotating single photon emission computer tomograph. Concomitant capnograph recordings showed that the end-expiratory pCO was higher during the rCBF than during the blood velocity examinations. This difference was highly significant. While there was no significant correlation between blood velocity and rCBF when these clear differences in pCO were disregarded, we did find significant positive correlations when the data were normalized to a standard pCO (5.3 kPa) using accepted formulas. The best correlation was found for the MCA (r=0.630, p<0.001) and the PCA (r=0.73, p < 0.001), with a lower correlation in the ACA (r=0.49, p<0.01) and the ICA (r=0.41, p<0.05). The estimated blood velocity (V) given rCBF=0 was not significantly different from 0. The results support the validity of expressing the relationship between blood velocity (V) and rCBF in defined cerebral artery systems as: V=1/60(rCBF) T (A), where A represents the area of the lumen of the vessel segment where the velocity is being measured, and T denotes the size of the brain region being perfused from this artery. [ABSTRACT FROM AUTHOR]

To study the pathologic and prognostic significance of—and possible underlying mechanisms for—a pathological exercise ECG in athletes, two age-matched groups were selected from a total population of 117 middle-aged and old endurance athletes: Group A: 21 with a pathological exercise-ECG, and group B: 21 with normal exercise-ECGs. Data from 201-thallium perfusion scintigraphy, 99 m-technetium multiple gated acquisition ventriculography (MUGA), resting echocardiography and 3 years follow-up are as follows: None had thallium findings indicating reversible myocardial ischaemia, but one from group A had a probable old myocardial infarction. All had normal resting MUGA, but group A men slightly more often presented a subnormal increase in ejection fraction according to exercise MUGA than group B men (9/20 vs 4/21). The former also more often had ventricular hypertrophy (LVH) (19/21 vs 14/21). However, apart from slightly longer ventricular filling time among group A men the echocardiograms revealed no group differences e.g. in cardiac dimensions or in indices of systolic or diastolic function. Regardless of exercise-ECG response,. 18/42 athletes had one or more value of left ventricular dimensions or diameter exceeding the 95th percentile of the normal range. Since one patient from group A had asymmetric septal hypertrophy, one developed cardiomyopathy during the 3 years follow-up and one had a previous myocardial infarction, only 3/21 had cardiac disease which might explain the pathological exercise-ECG. Thus, pathological exercise-ECG rarely signifies heart disease in athletes, and very rarely coronary heart disease. Rather, the pathological exercise-ECG may be related to L VH and various subtle alterations in cardiac physiology following long-term endurance training. [ABSTRACT FROM PUBLISHER]

Myocardial scintigraphy with thallium-201 and electrocardiogram-gated left ventriculography with technetium-99m labelled red blood cells were applied in four groups of subjects: 25 with no signs or symptoms of cardiovascular disease (group 1), 28 with a "false" positive exercise electrocardiogram (group 2), 14 with angina pectoris and normal coronary angiograms (group 3), and 43 with angina pectoris and fixed coronary artery stenoses (group 4). In groups 1 and 4 the radionuclide findings were in accordance with clinical and invasive measurements. In groups 2 and 3 the most important finding was the lack of increase in left ventricular ejection fraction during exercise in about half of these subjects (even a decrease in 25%), indicating subnormal myocardial reserve. The additional finding of pathological myocardial biopsies in four of these patients suggests that asymptomatic ST depression in patients with normal coronary angiograms may in some cases represent an early, preclinical sign of cardiomyopathy. [ABSTRACT FROM PUBLISHER]