The acute effects of ethanol (1.0 g/kg and 1.5 g/kg, n = 4 and n = 5, yielding blood concentrations of 1.3 +/- 0.2 mg/ml and 2.4 +/- 0.3 mg/ml) on myocardial perfusion were studied in anesthetized, thoracotomized, artificially ventilated dogs by using a radioactive microsphere technique. The control group (n = 5) received saline. The smaller dose of ethanol decreased perfusion in the left ventricular myocardium from 0.737 +/- 0.122 to 0.555 +/- 0.122 ml/g/min (NS), whereas the greater dose nonsignificantly increased it, from 0.744 +/- 0.115 to 0.819 +/- 0.119 ml/g/min (p
In experiments on the closed-chest dogs it was shown that NOS inhibition resulted in the significant alterations of hemodynamic indices (coronary and peripheral vascular resistance, cardiac output and heart rate) under local myocardial ischemia/reperfusion in comparison with control experiments. At the first time it was shown that NOS inhibition activated the autophagic destruction of cardiomyocytes in the ischemic myocardium and could reduce an area of functionally active myocardium. L-arginine administration attenuated cardio- and hemodynamic disturbances, that substantially improved the course of ischemia/reperfusion, diminished the ultrastructural changes in myocardium and prevented development of autophagic programmed cell death.
It has been suggested that the myocardium is able to recruit endogenous protective mechanisms in response to repeated ischemia and reperfusion. We set out to study whether this is manifested in patients with coronary artery disease in the form of fewer signs of myocardial ischemia during the second of two successive exercise tests and whether any relations exist between ischemia adaptation and findings at cardiac catheterization. Twenty-one patients with typical angina pectoris symptoms underwent two repeated bicycle exercise tests with identical protocols, followed by cardiac catheterization and coronary angiography the next day. The first exercise test was discontinued whenever a 2 mm ST depression in the electrocardiogram (ECG) was achieved or further exercise was limited by symptoms. The second exercise test was performed after disappearance of the symptoms or ST depression or both. Kaplan-Meier survival analysis for the appearance of a 1 mm ST depression demonstrated improved ischemia tolerance during the second test, when the required time for its appearance was significantly longer (6.5 +/- 0.8 min vs 4.5 +/- 0.5 min; p = 0.005). The maximal intensity of anginal pain was lower during the second exercise (2.2 +/- 1.0 min vs 0.7 +/- 0.3 min in Borg's scale; p
Angiogenesis is an essential biological process not only in embryogenesis, but also in the progression of several major diseases, including cancer, diabetes, and inflammation. Excessive vascularization can also contribute to some cardiovascular pathologies, such as atherosclerosis, but contradictory reports still prevail regarding its impact on aortic stenosis. Using immunohistochemical techniques, we assessed the vascular density and distribution of angiogenesis (FVIII) and vascular endothelial growth factor (VEGF) expression as well as the expression of 2 VEGF receptors, Flt-1 and Flk-1, in 55 nonrheumatic and 6 control aortic valves. In the light of the fact that the angiogenic effect of VEGF is mediated by sustained formation of nitric oxide, the samples were also immunostained with 3 nitric oxide synthase (eNOS, iNOS, and nNOS) antibodies. The immunohistochemical findings of VEGF and its receptors were verified by immunoblotting techniques. Vascular density was highest in the cases with moderate valve stenosis, and the mean number of FVIII-positive blood vessels was 1.7 +/- 1.9 vessels/mm(2) in the diseased valves, whereas the normal valves contained no blood vessels. Vascular density was significantly higher in the cases showing chronic inflammation (P = 0.007). Interestingly, the patients receiving statin therapy had significantly lower vascular densities than those not receiving such therapy (P = 0.001). Diseased valves showed distinct VEGF, Flt-1, Flk-1, and eNOS positivity of activated endothelial, stromal fusiform myofibroblastic, and histocytic cells. In contrast, immunoreactivity for iNOS and nNOS was seen only in nonendothelial stromal cells, and their expression was weaker. Enhanced vascular density was significantly associated with increased expression of Flk-1 (P = 0.028 for endothelial and P = 0.009 for stromal cells) and with endothelial eNOS expression (P = 0.024). A similar tendency was also observed for VEGF, but not for Flt-1. Our results show a distinct angiogenic response and the presence of angiogenic factors in nonrheumatic aortic valve stenosis, suggesting that angiogenesis may influence on the evolution of this disease.
The present study compared the clinical prediction of the effect of coronary artery bypass grafting (CABG) on coronary blood flow and left ventricular ejection fraction (LVEF) with changes in gated myocardial perfusion scintigraphy.
A prospective group of 92 patients underwent myocardial perfusion scintigraphy before and 6 months after CABG, the results being kept secret from the surgeon. Based on clinical and angiographic findings, the surgeons filled in a questionnaire indicating the predicted changes in coronary blood flow in each of the three coronary artery territories and in the LVEF.
Symptomatic improvement was present in nearly all the patients. Following CABG, the perfusion defects were reduced in around two-thirds and normalized in one-third of the territories clinically predicted to improve. Improved perfusion for territories not predicted to improve was slightly lower, and correlations between predicted and observed regional changes in coronary blood flow and perfusion defects were poor. LVEF increased (by over five ejection fraction units) in almost half of the patients, but with no correlation between the predicted and the observed changes.
Based on clinical and angiographic findings, the marked improvements after CABG in cardiac perfusion and function are poorly predicted.
A fibreoptic pressure sensor mounted on an 0.018 inch guidewire (Pressure Guide, RadiMedical Systems, Uppsala, Sweden) was used to measure the trans-stenotic pressure gradient in 20 patients admitted for percutaneous transluminal coronary angioplasty (PTCA) of a single, discrete stenosis. Pressure measurements were made both at rest and during maximal vasodilatation induced by intracoronary injection of papaverine. From the ratio of distal coronary pressure divided by the proximal pressure, the relative coronary flow reserve was calculated. The aim of the study was to compare the different pressure-derived parameters by correlating them to stenosis geometry estimated by quantitative coronary angiography. There was a moderate correlation between baseline pressure gradient and percent area stenosis; r = 0.64, P
BACKGROUND: The purpose of the study is to estimate the total blood flow in coronary artery bypass grafts. METHODS: In a 3-year period 102 patients having a standardized coronary artery bypass grafting (CABG) with the left internal mammary artery (LIMA) anastomosed to the left anterior descending artery and a sequential vein grafted to the remaining diseased coronary arteries were included in the study, 21 females and 81 males. In females a mean of 3.9 anastomosis (range 2-5) were performed and in males a mean of 4.2 (range 2-6) were performed. Flow in the bypass grafts was measured with the transit-time method before termination of cardiopulmonary bypass. RESULTS: Females: LIMA 31 mL/min, vein graft 74 mL/min (26 mL/min per anastomosis), cumulated flow 105 mL/min. Males: LIMA 31 mL/min, vein graft 93 mL/min (29 mL/min per vein anastomosis), cumulated flow 124 mL/min. CONCLUSION: Conventional CABG may restore half of the normal resting coronary artery blood flow (250 mL/min).
1 To identify the roles of endogenous kinins in prevention of myocardial infarction (MI), we performed the permanent ligation of coronary artery in rats. 2 The size of MI 12, 24, and 48 h after coronary ligation in kininogen-deficient Brown Norway Katholiek (BN-Ka) rats was significantly larger (49.7+/-0.2%, 49.6+/-2%, and 51.1+/-1%, respectively) than that of kinin-replete Brown Norway Kitasato (BN-Ki) rats (42+/-2%, 38.5+/-4%, and 41.5+/-1%). 3 Hoe140, a bradykinin (BK) B(2) receptor antagonist injected (1.0 mg kg(-1), i.v.) half an hour before, and every 8 h after, coronary ligation, significantly increased the size of MI in Sprague-Dawley rats. Aprotinin, a kallikrein inhibitor, which was infused intravenously (10,000 Units kg(-1) h(-1)) with an osmotic mini-pump, significantly increased the size of an MI 24 h after ligation. 4 When evaluated using microspheres, the regional myocardial blood flow around the necrotic lesion in BN-Ka rats 6 h after ligation was reduced more than that in BN-Ki rats with MI by 41-46%. The same was true in Hoe140-treated BN-Ki rats. 5 FR190997, a nonpeptide B(2) agonist, which was infused (10 microg kg(-1) h(-1)) into the vena cava of BN-Ka rats for 24 h with an osmotic mini-pump, caused significant reduction in the size of MI (38+/-3%), in comparison with the size in vehicle solution-treated rats (51+/-3%). The size of MI in FR190997-treated BN-Ka rats was the same as in BN-Ki rats. 6 These results suggested that endogenous kinin has the capacity to reduce the size of MI via B(2) receptor signalling because of the increase in regional myocardial blood flow around the ischaemic lesion.
Aortic valve calcification and stenosis become increasingly common with advancing age. This work aimed at assessing whether a time-dependent reduction of aortic valve area is detectable in an unselected elderly population and whether the rate of reduction can be predicted from clinical or biochemical characteristics.
A population-based prospective echocardiographic follow-up study.
A university hospital.
In 1990, randomly selected persons born in 1904, 1909 and 1914 (total n = 501) underwent a Doppler echocardiographic study of aortic valve and biochemical tests of glucose, lipid and calcium metabolism. In 1993, echocardiography was repeated in 333 survivors of the original cohorts. These individuals constitute the present study population.
Three-year changes in the aortic valve area and velocity ratio (peak outflow tract velocity/peak aortic jet velocity) determined by Doppler echocardiography.
Aortic valve area decreased from a mean of 1.95 cm2 (95% confidence interval of mean, 1.88-2.03 cm2) to 1.78 cm2 (1.71-1.85 cm2) within 3 years (P
OBJECTIVES We wanted to evaluate whether preoperative myocardial perfusion scintigraphy (MPS) could predict changes in cardiac symptoms and postoperative myocardial perfusion and left ventricular function after coronary artery bypass grafting (CABG). METHODS Ninety-two patients with stable angina pectoris (and at least one occluded coronary artery) underwent MPS before, and 6 months after, undergoing CABG. The result of the MPS was kept secret from the surgeons. RESULTS Before CABG, 90% of the patients had angina. After CABG, 97% of the patients were without symptoms. Overall graft patency was 84%. Before CABG, one patient had normal perfusion; in the rest of them the defects were classified as follows: reversible (60%), partly reversible (27%) and irreversible (12%). Following CABG, 33% had normal perfusion; in the rest the defects were reversible in 29%, partly reversible in 12% and irreversible in 26%. Left ventricular ejection fraction (LVEF), which was normal before operation in 45%, improved in 40% of all patients. The increase in LVEF was not related to the preoperative pattern of perfusion defects. Of 30 patients with normalized perfusion after CABG, 29 (97%) had reversible defects and one patient had partly reversible defects. Of 83 perfusion defects, which were normalized after CABG, 67 were reversible (81%) or partly reversible (12%). Seventy-five percent of all reversible coronary artery territories before CABG were normalized after operation. CONCLUSIONS Our results indicate that reversible or partly reversible perfusion defects at a preoperative MPS have a high chance of normalized myocardial perfusion assessed by MPS 6 months after operation. Normal perfusion is obtained almost exclusively in territories with reversible ischaemia. Symptoms improved in nearly all patients and LVEF in a significant fraction of the patients, not related to preoperative MPS.
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