Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Widely used non-invasive stress modalities, like exercise ECG, MPS and stress-echocardiography, are the tests of first choice for the diagnosis of CAD. It has been shown in numerous studies that non-invasive assessment of perfusion abnormalities is an adequate strategy for risk stratification. Moreover, non-invasive stress testing should be performed before a diagnostic cardiac catheterization to document the presence of myocardial ischemia, as a prerequisite for coronary revascularization. Coronary angiography is the gold standard for identifying CAD; however this technique is limited in assessing functional severity of coronary narrowings ('illusion of luminology'; see also Figure 5). The recently introduced i.c. hemodynamic parameters (CFVR and FFR) can identify functional severity of specific lesions and have shown a good agreement with the results of non-invasive stress test in validation studies. Furthermore, there is accumulating evidence that it is safe to defer a PTCA procedure, based on normal FFR and CFVR values. As these indices are derived during an invasive cardiac catheterization procedure, its use is recommended during a so called 'ad hoc' PTCA setting. Furthermore, they are particularly useful for clinical decision making in patients with documented multivessel CAD, as both indices allow selective evaluation of coronary narrowings in different arteries. Revascularization procedures are costly and always have a potential risk. It is important to be aware that, using above mentioned methods, unnecessary interventions (lacking potential benefit) may be avoided.
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PMID:Adequate patient selection for coronary revascularization: an overview of current methods used in daily clinical practice. 1213 22

The study was designed to assess the beat-to-beat variation of ventricular repolarization in patients with myocardial ischemia, hear failure, and in normal subjects. Autonomic tone may alter the dynamic QT/RR interval relation and thus may be involved in ventricular arrhythmia development, especially in the diseased heart. The study included 145 patients (age 16-86 years) with CHF (LVEF < or = 0.30) or unstable angina pectoris (LVEF > 0.60). The control group consisted of healthy volunteers giving physiological baseline measures for the evaluated parameters: cycle length, QT interval, and QT/RR interval ratio during three time periods. In patients with myocardial ischemia (LVEF > 0.60) and healthy subjects the QT/RR interval ratio did not reveal significant differences between both groups (QT/RR(CAD) = 0.36 +/- 0.77 vs QT/RR(controls) = 0.28 +/- 0.83; NS). In sharp contrast, in patients with severe heart failure, RR dependent instantaneous variation of the QT interval was almost missing and regression line analysis disclosed a QT/RR interval slope substantially enhanced by 196% (compared to normal subjects) and 131% (compared to CAD patients; P < 0.05) with a complete loss of circadian modulation (QT/RR(CHF) = 0.83 +/- 0.71 vs QT/RR(CAD) = 0.36 +/- 0.77 vs QT/RR(controls) = 0.28 +/- 0.83; P < 0.05). Beat-to-beat QT interval assessment provides a dynamic parameter of physiological and altered repolarization in defined study groups. Compared to other groups (preserved LVEF), patients with left ventricular impairment exhibited a significantly increased sensitivity of repolarization to cycle length (enhanced QT/RR interval ratio) and a blunted circadian modulation of the QT interval. This is consistent with concept that increased repolarization disparity may be deleterious being a potential pathophysiological basis for enhanced arrhythmic risk.
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PMID:Beat-to-beat assessment of QT/RR interval ratio in severe heart failure and overt myocardial ischemia: a measure of electrical integrity in diseased hearts. 1271 43

The most important adaptive responses from a physiological stance involved the cardiovascular system, consisting in particular of elevation of the cardiac output and its redistribution to favor the coronary and cerebral circulations, at the expense of the splanchnic vascular beds. The evidence regarding these physiological responses, especially in experimental studies that permit the control of many variables, is particularly powerful and convincing. On the other hand, there is a remarkable lack, in quality and quantity, of clinical studies addressing how normal physiological adaptive responses may be affected by a variety of diseases and conditions that often accompany and may complicate anemia, and interactions with other such compounding variables as age and different patient populations. For these reasons, it is not possible to offer guidelines on how to increase, maintain, or even to determine optimal DO2 in high-risk patients and how best transfusion strategies might be used under these conditions. From the brief review of physiological principles and the strong consensus in the literature, it is evident that cardiac function must be a central consideration in decisions regarding transfusion in anemia, because of the critical role it plays in assuring adequate oxygen supply of all vital tissues. Particular attention should be paid to the possible presence of CAD or incipient or cardiac failure, as these conditions may require careful transfusions to improve DO2 at levels that may not necessitate such interventions when cardiac disease is absent. Although the cerebral circulation also serves an obligate aerobic organ unable to tolerate significant hypoxia, there is little convincing evidence to support the notion that cerebral ischemia is aggravated by anemia and that this can be prevented by improved DO2 through rapid correction of anemia. Consequently, the arguments favoring transfusions in the presence of ischemic heart disease do not appear to apply to occlusive cerebrovascular disease. Because firm evidence is lacking on the interactions of concurrent diseases and anemia in various patient populations, understanding of the physiological consequences of anemia, and of the diseases concerned, is useful but not fully sufficient to provide firm and rational guidance to transfusion practice in specific complex clinical instances. A good deal of clinical and experimental investigation is required to support fully rational and comprehensive guidelines. In the meantime, prudent and conservative management, based on awareness of risks and sound understanding of the normal and pathological physiology, must remain the guiding principle.
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PMID:Physiologic aspects of anemia. 1513 60

In the last 50 years health care systems throughout the world have faced a new epidemic dual disease: cardiovascular disease (CVD)-diabetes mellitus. Nowadays, CVD is the leading cause of death in all western countries, and 60% of deaths for ischemic heart disease and stroke occur in developing countries with fixing resources. The striking association between CAD, stroke, peripheral artery disease and diabetes, since the publication of the first large-scale epidemiologic investigation in the 1970s, has forced physicians to investigate the possible pathophysiological connection among these diverse clinical conditions. Recent and compelling evidence has shown the significant and independent role of inflammation, insulin resistance and subsequent endothelial dysfunction in the initiation and progression of atherothrombosis, superimposed on traditional risk factors. Given the up-to-date molecular data linking diabetes, endothelial dysfunction, inflammation, and atherosclerosis, this review will focus on the common mechanisms underlying these conditions and on new promising therapeutic strategies.
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PMID:Diabetes and inflammation. 1559 71

The currently best available spatial and temporal resolution for retrospectively ECG gated coronary multi-detector-row CT angiography is 0.4 mm and 165 ms, respectively. These acquisition parameters are already rather close to cardiac catheter. Studies so far compared non-invasive coronary CT and convention angiography for the detection of coronary artery stenoses. The most promising result reported by all authors was the high negative predictive value of the CTA. It now needs to be determined if CTA is a reliable tool to rule out coronary artery stenoses in a patient cohort with low likelihood of CAD, such as those with atypical chest pain or ambiguous stress test. CTA may furthermore establish as a rapid and widely available tool to detect vulnerable plaques or intracoronary thrombus in patients with acute coronary syndrome and unstable angina. In patients with chronic stable angina, tools that determine myocardial ischemia under stress such as SPECT and MRI are probably better suited to determine the relevance of coronary artery stenoses. In this particular cohort, by displaying the extent and morphology of coronary atherosclerosis, CTA may help to direct the therapy to either intervention or surgery.
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PMID:Coronary CT angiography in symptomatic patients. 1580 Oct 55

This study compared the effects of long-term administration of nicorandil and isosorbide dinitrate (ISDN) on vascular endothelial function and the progression of arteriosclerosis. Forty-two patients with ischemic heart disease were randomly allocated to receive nicorandil (N group; 15 mg/d) or ISDN (I group, 40 mg/d). Twelve normal subjects served as controls. Vascular endothelial function and the progression of arteriosclerosis (intima-media thickness, IMT), as determined by carotid vascular ultrasound, were assessed 1 week before and 3 months after drug administration. Reactive hyperemia was induced in the forearm for 5 minutes, and the percentage change in the diameter of the brachial artery (% change in flow-mediated dilation, %FMD) was calculated. FMD was significantly lower in CAD groups than in controls. The %FMD significantly decreased (7.2 +/- 1.9 to 4.2 +/- 2.8) in the I group, while rising from 6.8 +/- 1.6 to 8.0 +/- 2.0 in the N group. IMT increased by 0.036 +/- 0.015 mm in the I group but showed no significant change in the N group (-0.01 +/- 0.012 mm). Thus, ISDN deteriorates IMT and FMD, whereas a beneficial effect of nicorandil is seen on FMD with no effect on IMT. Long-term treatment with nicorandil may be desirable for prevention of cardiovascular events.
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PMID:Effects of the long-term administration of nicorandil on vascular endothelial function and the progression of arteriosclerosis. 1596 56

NSTE-ACS is a complex clinical event characterized by a variable degree of myocardial ischemia and triggered, in most patients, by a rupture of a vulnerable plaque that leads to acute intraluminal nonocclusive thrombosis. Traditionally, acute management strategies for NSTE-ACS have been aimed at identification of vascular areas with discrete atheroma and revascularization of the affected myocardium. Studies that have evaluated invasive strategies in NSTE-ACS suggest that the rates of hard clinical events are similar for both intensive medical treatment and early invasive management strategies. As shown recently in the Cooperative Cardiovascular Project study, intensive therapy with beta-blockers appears to be a viable management option that has comparable outcomes in most patients with NSTE-ACS. Although several different treatment strategies have been advocated in the management of NSTE-ACS, the available evidence-based information does not fully support some of these traditional approaches. Future prospective, well-controlled trials are needed to fully ascertain the role of invasive and other medical management strategies in patients with NSTE-ACS. Long-term aggressive management of established risk factors for CAD is unquestionably the most prudent and cost-effective therapeutic approach in the long-term management in patients recovering from NSTE-ACS.
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PMID:Treating non-ST-segment elevation ACS. Pros and cons of current strategies. 1620 5

Systemic factors and blood flow velocity related to atherosclerosis have been examined mainly separately or by in vitro studies. The aim of our study was to investigate the association between local coronary blood flow (corrected TIMI frame count, CTFC) and systemic atherosclerosis-related inflammatory parameters such as soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (Il-6), high sensitivity C-reactive protein (hsCRP) and von Willebrand factor (vWF) in humans. We enrolled the following groups of ischemic heart disease (IHD) patients: patients with coronary stenosis and stable (CAD, n = 96) or unstable angina (ACS, n = 27), patients with documented myocardial ischemia and normal coronary angiogram (NEG, n = 68). Patient groups showed only marginal differences in CTFC or sICAM-1 levels. In contrast, when IHD patients were studied individually, general positive correlation was found between CTFC and sICAM-1 level (r = 0.33; in NEG r = 0.25; in CAD r = 0.37; in ACS r = 0.61), being the strongest in ACS. The relation was independent from age, gender, BMI, smoking, hypertension, diabetes, previous myocardial infarction, family history of IHD, medication, hsCRP, IL-6 and vWF levels. (odds ratio, OR = 6.4; CI 95%: 2.43-16.84; p < 0.05). Nevertheless, correlation between CTFC and IL-6, hsCRP, vWF levels was not found. These results indicate inverse correlation between coronary blood flow and adhesion molecule production independently from conventional cardiovascular risk factors and inflammatory markers.
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PMID:Inverse correlation between coronary blood flow velocity and sICAM-1 level observed in ischemic heart disease patients. 1629 92

This was an observational study carried out in the department of cardiology. Bangabandhu Shikh Mujib Medical University (BSMMU), Dhaka in collaboration with Institute of Nuclear Medicine (INM), Shabag, Dhaka during the period October 2002-March 2003. A total of 54 patients presenting with Canadian Cardiovascular Society (CCS) class I-II severity of chest pain with mean +/-SD age 49.88 +/- 8.44 yrs and having male to female ratio 5.75:1 were included in the study. The main objective of the study was to predict severity of myocardial ischemia by Exercise Tolerance Test (ETT) determined by Duke Treadmill Score (DTS) and by perfusion pattern observed following Single-Photon Emission Computed Tomography myocardial perfusion imaging (SPECT-MPI). All patients underwent ETT and then SPECT-MPI scan using Tc-99m-tetrofosmin in one-day stress and rest protocol. Coronary angiogram (CAG) was done with in six months of the perfusion study. After performing ETT, patients were categorized by DTS and myocardial perfusion studies were also stratified according to severity of perfusion defect. The formula used to calculate the score was: Exercise time- (5 x ST segment deviation)-(4 X Treadmill angina index). The angiographic findings (significant >50% stenosis) and perfusion defects in MPI were compared with the severity of DTS. There were 31 patients who had CAG proven (>50% luminal diameter narrowing) CAD and 23 patients free of CAD. After ETT patients were categorized by Duke Treadmill Score into high DTS 12 (22.22%) patients, intermediate DTS 20 (37.03%) patients low DTS 22 (40.74%) patients. In high DTS group 91.66% patients had perfusion defect, whereas in intermediate and low risk group it was 60% and 40.9% respectively. In high DTS group 91.66% of patients had angiographicaly proven CAD, 58.33% of them had triple vessel disease (TVD) while in intermediate and low risk groups angiographically proven CAD were 65% and 22.72% of whom TVD only in 15% & 0% respectively. The results of ETT using DTS score were satisfactorily correlated with SPECT-MPI scanning in high DTS subsets of patients only. It is therefore, suggested that patient of high risk DTS do not need for myocardial perfusion imaging study and should undergo CAG for further evaluation. But the intermediate and low risk groups were needed myocardial perfusion imaging study to guide for further evaluation.
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PMID:Role of exercise tolerance test (ETT) and gated single photon emission computed tomography-myocardial perfusion imaging (SPECT-MPI) in predicting severity of ischemia in patients with chest pain. 1668 38

Myocardial ischaemia is known to be significantly related to the development of coronary collaterals, but there are considerable variations in their formation. The nature of this variability is not well understood. Likewise it remains unclear whether diabetes mellitus. DM has any effect on coronary collaterals. The aim of this study was to evaluate the effect of diabetes mellitus on coronary collaterals. This prospective case- control study was done from January to December 2000 in patients undergoing coronary angiography in National Institute of Cardiovascular Diseases (NICVD), Dhaka, who fulfilled the inclusion criteria of having < or = 75% stenosis in at least one coronary artery. The patients with diabetes having CAD without other modifiable major risk factors (hypertension, smoking, dyslipidaemia) were constituted case study group (n=36) and nondiabetic patients having CAD with those risk factors were constituted control group (n=50). Coronary collaterals were graded according to Rentrope scoring system and the collateral score was calculated by summing the Rentrope number of every patient. There was no statistical difference between patients with and without diabetes in clinical characteristics. The mean number of diseased vessel in DM group 2.6+/-0.6 was higher than that in nondiabetic patients (2.1+/-0.8, P>.05). The mean collateral score was 0.5+/-0.6 in DM group and 1.2+/-1.0 in nondiabetic group. These findings suggest that coronary collateral development is significantly poorer in diabetic than on diabetic patients.
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PMID:Comparative study of coronary collaterals in diabetic and nondiabetic patients by angiography. 1687 99


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