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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After an extensive analysis of the world literature (121 references), beginning from the first reported case by Antopol and Kugel, 1933, the general review of the problem stressed especially the following morphologic characteristics and clinical significance of the anomalous origin of the left circumflex coronary artery (LCxA) from the right coronary artery (RCA): The place of the anomalous origin of LCxA from RCA among all other variations and anomalies of LCxA. The anatomical and topographical characteristics of LCxA originating from RCA in normal heart as well as in congenital heart diseases--CHD (especially complete transposition of great arteries--TGA). The formal genesis of LCxA from RCA according to original new Ogden's theory, taking into account the dual origin of the coronary arteries and the peritruncal angioblastic ring that surrounds the developing aorta and pulmonary artery. The frequencies of the origin of LCxA from RCA in autopsy and coronarography series. The importance of LCxA (by its origin and/or caliber) in determination of the right, left or codominance of the coronary arteries including the peculiarities in cases of isolated aortic stenosis and bicuspid aortic valve. The importance of recognizing LCxA from the RCA during implantation of artificial aortic, mitral and tricuspid heart valves, during mitral valve anuloplasty, closure of ostium primum defect as well as during aorto-coronary venous bypass. The LCxA from RCA, especially its proximal segment, shows more frequent and an earlier, faster and heavier obstructive atherosclerosis, causing different manifestations of coronary heart disease and sudden death. Also, mitral insufficiency can be caused by ischemia of the papillary muscles of the left ventricle. The awareness of the possibility that LCxA may arise from the RCA can prevent many complications during cannulations of the coronary arteries for diagnostic coronarography and myocardial perfusion during heart operations. The authors presented their 30 autopsied cases of LCxA from RCA, analysing morphological and topographic data as well as their clinical significance and association with other CHD. There were 6 isolated cases and 24 cases associated with other CHD (20 with TGA and 4 with other CHD). Our first autopsied case of LCxA from RCA was diagnosed as associated with tetralogy of Fallot in 1964. During the period 1964-1985 we had 1015 cases of CHD (including 132 cases of TGA).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathologic morphology and clinical significance of the anomalous origin of the left circumflex coronary artery from the right coronary artery. General review and autopsy analysis of 30 cases]. 213 27

Balloon dilatation was used to explore the strength of the left ventricular wall in rats. The rupture pressure of the left ventricle was 645 +/- 22 mm Hg and that of the right ventricle was 247 +/- 15 mm Hg in intact animals. Left ventricular hypertrophy induced by 50% ascending aortic stenosis increased rupture pressure proportionally to the degree of hypertrophy. In transmural myocardial infarction occupying 40-55% of the left ventricular wall volume, the rupture pressure within 10 days of myocardial infarction was the same as that in the intact myocardium. Following 24 hours of ischemia, myocardial reperfusion produced no effects, but after 2 or 4 hours of ischemia it reduced the strength of the heart wall by 50%. It was concluded that early thrombolytic therapy might be a risk factor for cardiac rupture in myocardial infarction.
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PMID:[The role of myocardial reperfusion and hypertrophy in the development of heart rupture in experimental myocardial infarction]. 213 4

Eighteen dogs underwent transmural left ventricular biopsies for adenosine triphosphate and suturing of the noncoronary cusp, creating valvular aortic stenosis. Three months after aortic stenosis and the subsequent development of left ventricular hypertrophy, animals underwent repeat transmural left ventricular biopsies followed by total myocardial ischemia at 37 degrees C. Left ventricular tissue samples for adenosine triphosphate and lactate levels were determined at 15-minute intervals and compared with 15 control animals. No significant difference between subendocardial and subepicardial adenosine triphosphate levels was found between left ventricular samples taken before left ventricular hypertrophy and 3 months after left ventricular hypertrophy. Significant differences in adenosine triphosphate utilization occurred between subendocardial and subepicardial layers in control and left ventricular hypertrophy myocardium, however. The gradient between the subendocardium and the subepicardium was significantly increased by left ventricular hypertrophy (p less than 0.05). Significant differences also occurred within the same layer when left ventricular hypertrophy and control groups were compared. During total ischemia, lactate concentration was significantly greater within the subendocardium than within the subepicardium in left ventricular hypertrophy. The onset of ischemic contracture was 48.2 +/- 2.1 minutes in left ventricular hypertrophy versus 62.3 +/- 1.8 minutes in control hearts (p less than 0.01). Subendocardial intramyocardial pressure increased significantly earlier than subepicardial in both left ventricular hypertrophy and control hearts. Adenosine triphosphate was used, and lactate accumulated more rapidly in animals with a more pronounced hemodynamic gradient. These data show that after left ventricular hypertrophy, adenosine triphosphate stores in the subendocardium and the subepicardium are unchanged from control values, yet the rates of adenosine triphosphate utilization and lactate accumulation during total ischemia are significantly increased. Furthermore, the subendocardial to subepicardial gradient of adenosine triphosphate utilization during ischemia found in normal hearts is markedly increased by left ventricular hypertrophy.
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PMID:Accelerated transmural gradients of energy compound metabolism resulting from left ventricular hypertrophy. 214 78

Recent investigations in several organs indicate cytoprotective effects of prostanoids. For further elucidation of this efficacy the investigations dealt with the cardioprotection of prostanoids (iloprost, PGE1) and the cyclooxygenase inhibitor indomethacin under in vivo- and in vitro-conditions. The experiments were carried out in isolated perfused guinea pig hearts and anaesthetized rabbits. Cardiac damage was induced by chemical substances or loading by aortic constriction or ischemia. In isolated perfused hearts iloprost and indomethacin suppressed the toxic effects of carbon tetrachloride, chloroform, benzene, sodium dithionate and phenylethylbarbituric acid, but not the efficacy of quinine sulfate and 2,4-dinitro-phenol. Cardiac loading by aortic stenosis or ischemia induced a decrease of contractility and blood pressure and changes in the myocardial PGI2-biosynthesis. On the other side application of indomethacin, iloprost or PGE1 diminished the cardiac damage and inhibit the myocardial PGI2-formation. The results show that indomethacin and prostanoids have a protective effect in pathophysiological changes or toxic damage of the heart, possibly caused by a stabilization of the cellular membrane.
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PMID:Significance of the cardioprotective effect of prostanoids and indomethacin. 247 Mar 59

In hypertensive heart disease without coronary artery disease it has been proposed that the presence of ischemia of myocardial tissue is due to an inadequate increment of myocardial mass or to an increase in coronary artery resistance. In this study, 18 patients with aortic stenosis, without coronary artery disease were included. It was demonstrated that the existence of myocardial ischemic, induced by atrial pacing and manifested by ST segment depression, had direct association to increased myocardial mass, and it had no relation with left ventricular telediastolic pressure nor with transvalvular gradient. The results support the hypothesis that an inappropriate increment of the myocardial mass is the main cause of myocardial ischemia in these type of cardiopathies.
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PMID:[Myocardial ischemia in aortic stenosis]. 253 25

The effects of balloon inflation on myocardial perfusion and metabolism were studied during aortic valvuloplasty in 17 patients with aortic stenosis, including 6 with associated coronary artery disease. Coronary sinus flow and blood samples were obtained before and during the first inflation, and 5 to 10 minutes after the last inflation. During inflation, coronary blood flow decreased (272 +/- 111 standard deviation to 166 +/- 92 ml/min; p less than 0.05), myocardial oxygen uptake fell and transcardiac lactate handling shifted from extraction to production (35 +/- 54 to -41 +/- 48 mumol/min; p less than 0.01). At the end of the procedure, aortic valve area had increased from 0.51 +/- 0.22 to 0.81 +/- 0.48 cm2 (p less than 0.002). Coronary sinus flow increased slightly above control values (+6%; difference not significant) and myocardial oxygen and lactate uptakes were back to control values. However, myocardial alanine production had increased from -3.6 to -6.6 mumol/min (p less than 0.05) and glutamine production was reduced or replaced by extraction (-3.3 +/- 2.1 to 3.5 +/- 3.8 mumol/min; p less than 0.05). Recovery of coronary flow, oxygen and lactate uptakes was not significantly different in patients with or without coronary artery disease, although the former patients tended to have less glutamine extraction and less improvement in their ejection fraction at the end of the procedure. Thus, aortic balloon valvuloplasty produces brief episodes of low-flow ischemia. Recovery of oxidative metabolism is almost immediate after deflation and no detrimental effect seems to persist at the end of the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in coronary blood flow and myocardial metabolism during aortic balloon valvuloplasty. 296 50

Cardiac tissue from different parts of hearts from guinea pigs and rabbits have the capacity to rapidly synthesize prostacyclin (PGI2). Auricles show a higher PGI2-formation than ventricles. Addition of the endoperoxide PGH2 markedly enhanced the myocardial PGI2-biosynthesis. Furthermore many cardiotonic drugs induced a significant rise, but eicosanoids or cyclooxygenase inhibitors a marked reduction of the cardiac PGI2-formation. Acute pressure overload by graduated aortic stenosis, ischemia by coronary ligation or pacing with high frequency reduced the cardiac contractility. After aortic stenosis the myocardial PGI2-biosynthesis is lowered, but increased after coronary ligation or pacing. Under these conditions indomethacin, PGE1, iloprost, verapamil and trapidil markedly reduced the PGI2-biosynthesis and exert a protective effect in regard to cardiac damage. The results indicate that pathophysiological changes significantly influence the PGI2-biosynthesis of the heart. The drug induced inhibition of the myocardial PGI2-formation parallels a cardioprotective effect of these substances.
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PMID:Myocardial biosynthesis of prostacyclin and the influence of cardiac loading and drugs. 307 64

Clinical studies of patients with aortic stenosis suggest that left ventricular myocardial injury is frequent. To examine the morphologic basis of this observation, we studied 32 patients with isolated aortic stenosis, no cardiac surgery, and hearts studied at autopsy after postmortem arteriography and fixation in distension. The patients were 46-87 years old (average 69), and 21 (66%) were male. Calcific aortic stenosis was present in 19 hearts, 12 had congenital bicuspid aortic valve, and 1 had rheumatic aortic stenosis. In 19 hearts there was moderate or marked coronary atherosclerosis, and 12 hearts had 17 myocardial infarcts. However, among 13 hearts with no or mild coronary atherosclerosis, 9 had either subendocardial myocardial contraction band necrosis, a lesion occurring when periods of no perfusion are followed by reflow, or focal replacement fibrosis. In 13 hearts there was subendocardial vacuolization of myocytes, an alteration produced by ischemia, that was not accounted for by coronary artery disease. Our results are consistent with clinical observations and show that ischemic myocardial injury may be associated with isolated aortic stenosis in the absence of coronary artery obstruction. The contraction band necrosis and vacuolated myocytes suggest that both episodic and sustained reductions of subendocardial blood flow occur in the presence of aortic stenosis.
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PMID:Myocardial injury in patients with aortic stenosis. 345 33

As a result of improvement in intraoperative and postoperative management, severe aortic valve disease can be cured by operation, however, late cardiogenic sudden death after aortic valve replacement (AVR) has been existed as one of the important unsolved problem. This report is aimed to predict the risk factors influencing the postoperative prognosis of severe aortic valve disease. Twenty-three cases with aortic regurgitation (AR) and 20 cases with aortic stenosis (AS) were selected by postoperative period over 12 months. In 18 AR cases with normal coronary artery substantiated by selective coronary angiography, cross sectional area index of left ventricular wall (CSAI) and ST depression in left chest leads of electrocardiogram correlated well as the CSAI increased, so decreased the ST segment. This shows the increment of CSAI leads left ventricular endocardial ischemia. By means of introduction of this indicator, 23 AR and 20 AS patients were divided into two groups as group C-I having CSAI over 20 cm2/m2 and group C-II under 20 cm2/m2. Left ventricular ejection fraction (EF) was selected as an predictive indicator of left ventricular function. As same as CSAI, AVR cases were divided into two groups as group E-I having EF under 50% and E-II over 50%. Each group was compared concerning with the complication rate of postoperative low cardiac output syndrome (LOS) and late cardiogenic sudden death. In C-I group of AR, 55% cases accompanied with LOS, 18% died due to LOS and 18% died suddenly from late cardiogenic cause, however, none of cases in C-II group had these complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Risk factors influencing the prognosis of severe aortic valve disease following aortic valve replacement]. 369 58

Ear lobe creases have been proposed as useful indirect markers of coronary artery disease. To test such a hypothesis, this physical sign was evaluated in 100 patients with symptomatic aortic stenosis undergoing cardiac catheterization to establish the hemodynamic severity of the obstruction and the degree of coronary artery involvement. This is a disorder where the coexistence of cardiac ischemia may play an important part in diagnosis and management. Criteria were established for the degree of ear lobe involvement with a grading of mild (Grade 1), moderate (Grade 2), and severe (Grade 3). Significant coronary artery disease was defined as narrowing greater than or equal to 50% and a coronary score was established. Sensitivity, specificity, positive and negative predictive values were calculated, using Bayesian analysis for three levels of assumed coronary artery disease prevalence. An ear lobe crease score was correlated with a coronary artery disease score, taking into account the variables of age, sex, and body mass index. No useful statistical correlations were found and it is concluded that this physical sign is of little practical value in this clinical setting.
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PMID:The ear lobe crease sign and coronary artery disease in aortic stenosis. 373 65


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