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At least 703 records · Page 39Linked to original sources
PubMed2006

Challenges in the phenotypic characterisation of patients in genetic studies of coronary artery disease.

Coronary artery disease and acute myocardial infarction are complex traits in which there has been recent research to identify the principal genes that engender susceptibility or provide protection. Although there has been exceptional progress in the technology, which now allows genotyping of hundreds of thousands of single-nucleotide polymorphisms in each individual, there remains a pattern of inconsistency in the studies performed to date, in part owing to the difficulties in defining cases and controls. In this paper, salient issues to facilitate research in this important field are reviewed.

Adolescent↗
PubMed1975

[Hemodynamic differences between maximal treadmill and bicycle ergometer test in coronary disease].

9 patients with diagnosis of coronary heart disease (CHD) and typical angina pectoris (AP) were studied by means of a multistage, symptom-limited treadmill test and a similar bicycle ergometer (bike)-test. The sequence of tests was determined by chance. Between the tests, the patients rested one hour. Oxygen uptake (vo2) was determined by the Douglas-bag-method, blood pressures were measured via catheters placed in a pulmonary and a brachial or radial artery, respectively. Cardiac output (Q) was calculated by the direct Fick principle. In all tests, with the exception of one bike-test, all patients were limited by AP. They attained high VO2 (mean 1316 ml/min) on the treadmill (TM) while on the TM their mean arterial blood pressure (BP) was significantly (P greater than 0.05), namely 10 mm Hg as an average, lower. Comparing the final minute -3 of the TM-test with the final minute -1 of the bike-test in 5 patients, we found heart rate (HR), BP and pressure rate product (HR times BP) lower on the TM (P greater than 0.05), whereas VO2 was the same. Patients, whose exercise performance is limited by angina pectoris on bike and TM, achieve higher VO2 on the treadmill, together with lower BP. This may be of clinical importance in exercise-testing and -training of patients with CHD.

Aerobiosis↗
PubMed1997

[Rationale for lipid therapy. Prevention or treatment of coronary heart disease?].

Coronary artery disease has still a grave prognosis. More than half the patients die within 24 hours, mostly before reaching a hospital. A minority survives the first year. Only more intense prevention will change this. Primary prevention in a narrow sense refers to the prevention of the development of early lesions in the youth and as such is a responsibility of the education towards a healthy lifestyle. In our population a majority of middle-aged is likely to have developed arteriosclerosis, so that we deal only with clinically defined primary prevention even though they are asymptomatic. The outstanding effects of lipid therapy in patients at risk for coronary heart disease will primarily result from avoiding the development of instable plaques. Reduction of LDL-cholesterol and increase of HDL-cholesterol is most effective in patients with proven coronary artery disease. Evidently the majority of coronary events can be prevented by idealizing the lipid parameters. In contrast, the chronic coronary syndrome is the domain of the interventional cardiology. Lipid therapy will lead only gradually to a reduction of significant coronary stenoses. However, there is the still insufficiently investigated potential of improving the endothelial dysfunction by correcting the lipid metabolism to reduce angina.

Anticholesteremic Agents↗
PubMed2001

Mechanisms of plaque stabilization for a charged calcium channel blocker in coronary artery disease.

Coronary artery disease (CAD) results from atherosclerosis, a systemic vascular disorder that is the leading cause of death and disability throughout much of the developed world. Because cellular changes associated with vulnerable atherosclerotic plaque are characterized by a loss of normal calcium regulation, there is strong interest in a potential antiatherosclerotic role for calcium channel blockers. This hypothesis has been supported by investigational studies conducted in well-defined cellular and animal models of atherosclerosis. In addition, several clinical studies have tested the benefit of calcium channel blockers among patients with mild-to-moderate CAD. More recent trials have shown reductions in cardiovascular events after treatment with amlodipine, a long-acting, dihydropyridine-type calcium channel blocker. The Prospective Randomized Evaluation of the Vascular Effects of Norvasc Trial (PREVENT) demonstrated that patients with documented CAD treated with amlodipine experienced marked reductions in cardiovascular events compared with patients receiving placebo. Amlodipine also was associated with significant slowing of carotid atherosclerosis, an important surrogate marker for CAD, independent of blood pressure modification. These results have renewed interest in potential plaque stabilization properties of third-generation calcium channel blockers and their possible therapeutic role in CAD.

Amlodipine↗
PubMed1998

Carotid and coronary disease: staged or simultaneous management?

Up to 12% of patients presenting for coronary bypass have critical carotid disease, and more than 50% of patients presenting for carotid endarterectomy have significant coronary disease. Patients requiring surgery for both carotid and coronary disease may be managed with carotid endarterectomy followed by coronary bypass (staged approach), with coronary bypass followed by carotid endarterectomy (reversed staged approach), or with simultaneous coronary bypass-carotid endarterectomy. There are no compelling data proving superiority of any of these three approaches. The staged approach is usually associated with lower stroke rates but higher myocardial infarction and mortality rates; the reversed staged approach with higher stroke rates but lower myocardial infarction and mortality rates; and the simultaneous approach with intermediate stroke, myocardial infarction, and mortality rates. Unfortunately, reported series vary widely in stroke and mortality rates because of wide variability in patient selection criteria, especially for simultaneous procedures. Management decisions in these patients should be based on the relative severity of their carotid and coronary lesions. Management guidelines are discussed in detail.

Carotid Artery Diseases↗
PubMed1997

[Factors determining the improvement of effort capacity in aged patients with coronary disease during the 1st month following coronary surgery].

UNLABELLED: In order to determine the predictive factors of improvement of the physical capacity of elderly coronary patients following coronary surgery, we retrospectively analysed the data of 204 consecutive patients over the age of 65 years (181 men, 23 women, mean age: 70 +/- 4.4 years), admitted for a phase II active training programme. METHODS: The patients were divided into two groups as a function of the rate of improvement of the duration of the stress test: group A (improvement greater than or equal to 25%; n = 108) and group B (less than 25%; n = 96). Comparison of these 2 groups by multivariate analysis identified predictive factors of improvement among seven variables: age, sex, excess weight, haemoglobin, number of training sessions, duration of baseline stress test, interval between bypass graft and start of training. RESULTS: After training, the duration of the stress test and the maximal power were improved by 26.5% and 24%, respectively: 7.1 +/- 1.7 vs 8.9 +/- 2.3 minutes (p = 0.0001); 79 +/- 18.4 vs 97.8 +/- 23.7 watts (p = 0.0001). 34 (1.4%) of the 2,396 training sessions were temporarily interrupted, because of muscle fatigue in 47% of cases. Patients who had readapted before the 15th postoperative day presented fewer incidents: 4.3% vs 13.1%; NS. Only three variables appeared to be predictive of improvement of physical capacity: a duration less than 6 minutes on the baseline stress test (p = 0.0003), more than 12 training sessions (p = 0.0029) and age less than or equal to 70 years (p = 0.014). CONCLUSION: In elderly subjects undergoing coronary surgery, the improvement of physical capacity is greater the lower the baseline effort, the lower the age-group and the greater the number of training sessions. In the absence of contraindication, it appears justified to include elderly coronary patients in training programmes, even when their baseline effort level appears to be low. This training can be started by the 15th postoperative day.

Age Factors↗
PubMed1992

Low density lipoprotein composition and oxidizability in coronary disease--apparent favourable effect of beta blockers.

The oxidative modification of LDL in vivo may have an important role in atherogenesis. To determine whether LDL fatty acid, anti-oxidant composition and sensitivity to oxidation in vitro is different in subjects with established atherosclerosis we compared 20 men with angiogram proven coronary disease with 25 controls without clinical evidence of arterial disease. LDL-cholesterol, total triglycerides and LDL fatty acid composition did not differ significantly between the groups. LDL oxidation lag time and oxidation rate in coronary patients (132 min, 0.02 absorbance units/min) and controls (140, 0.017) were not significantly different. However coronary disease subjects taking beta-blockers had evidence for reduced LDL oxidizability (lag time 148 +/- 7 min; oxidation rate 0.017 +/- 0.002 abs units/min) compared with those not on beta-blockers (lag time 114 +/- 7 min, rate 0.025 +/- 0.003, P < 0.005). LDL beta-carotene was significantly lower in coronary patients (0.92 mumol/mmol LDL cholesterol; controls 1.58; P = 0.001). LDL alpha-tocopherol appeared lower in coronary patients (2.8 mumol/mmol LDL cholesterol; controls 3.3; P = 0.056) and was significantly lower in smokers (2.56; non-smokers 3.24; P = 0.04). LDL oxidation rate was negatively correlated with LDL alpha-tocopherol (r = -0.51, P = 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1992

The hypertrophied myocardium and coronary disease. Structural changes in patients submitted to aortocoronary bypass surgery.

Seventeen patients with coronary disease submitted to myocardial revascularization were studied. Ten patients had a hypertrophied ventricle, and 7 had normal ventricular mass. Myocardial biopsies were obtained before ischemia and at the time of reperfusion and were assessed for: volume fraction of fibrous tissue, myocyte diameter, morphometric mitochondrial studies and ultrastructural changes. The volume fraction of fibrous tissue in patients with hypertrophied ventricle was 1.9 +/- 0.04, and in patients with normal ventricular mass was 0.9 +/- 0.01 (p less than 0.05). The diameter of the myocyte was 23 +/- 0.3 microns and 18 +/- 1.2 microns for patients with hypertrophied and normal ventricular mass, respectively (p less than 0.01). The value of volumetric density for pre-ischemia samples in patients with a hypertrophied ventricle was 23 +/- 2.2 and in patients with normal ventricular mass was 35 +/- 2.7 (p less than 0.02). Grades 3 and 4 of damaged mitochondria were significantly increased in reperfusion samples from patients with a hypertrophied ventricle compared to pre-ischemia samples. Collagen growth was increased in hypertrophied hearts which were also more sensitive to the ischemia/reperfusion mechanism.

Biopsy↗
PubMed1984

The different radionuclide angiography (RNA) responses to upright bicycle ergometer exercise in a population with low probability coronary disease.

One hundred and one subjects (52 men, 49 women) with low probability coronary disease and normal resting left ventricular ejection fraction performed upright bicycle exercise to target without angina, ischemic ECG change, or segmental wall motion abnormality. Fifteen millicuries of Tc-99m pertechnetate were injected at rest and during peak exercise, and images were processed with first pass technique (RNA). The responses were not uniform. Group 1 was characterized by the resting end diastolic volume index (EDVI) usually greater than 80 ml/M2, a peripheral resistance drop (decreases R) of 0.20-0.50, an increase in cardiac index (increases CI) of 2.8-5.5 1/minute/M2, accompanied by decreasing EDVI and ESVI with exercise, stroke volume index (SVI) remaining essentially unchanged, and left ventricular ejection fraction (EF) usually increasing. Group 2 was characterized by the resting EDVI less than 80 ml/M2, and with the same decreases R and increases CI; EDVI, ESVI, SVI all increased and EF tended to decrease. Group 3 was characterized by decreases R greater than 0.50, increases CI greater than 5.5 1/minute M2, the exercise EDVI usually increasing, ESVI usually decreasing, SVI usually increasing, and EF usually increasing. There were no significant differences (alpha = 0.01) in exercise-related changes between men and women within each group.

Blood Pressure↗
PubMed1997

Evidence of multifocal activity of coronary disease in patients with acute myocardial infarction.

BACKGROUND: Destabilization of the fibrous cap facilitates plaque rupture, thrombus formation, and myocardial infarction. Because systemic stimuli, such as lipoproteins, infectious agents, and autoantigens, may incite this reaction, one may wonder whether disruption mechanisms are only local or systemic and infarction is caused by an arbitrary plaque event or by a systemic, acute activity of the coronary disease. METHODS AND RESULTS: Early (3 to 5 days) and late (1 month) peri-infarction coronary angiographic data in 23 patients with first infarction were compared with that in 23 similar patients, with angiography performed because of stable angina and repeated after 1 month before angioplasty. Nonculprit lesion changes at the narrowest point defined progression or regression when exceeding 0.27 mm. In patients with recent infarction we found that 16 had progression, 4 had regression, 1 had both, 2 were steady (values in patients with stable angina being 2 [P<.0011, 1 [NS], 0 [NS], and 20 [P<.001]); 27 lesions were infarct related; 17 of the 45 nonculprit lesions progressed and 5 regressed (values in stable angina being 2 [P<.001] and 1 [P<.05] out of 78); minimal diameter reduction of progressing stenoses averaged 0.39 mm; lumen increase of regressing lesions averaged 0.30 mm; 3 patients developed interim rest angina associated with progression of a nonculprit lesion. CONCLUSIONS: A greater proportion of subjects and lesions with progression or regression (in infarction versus stable angina) supports the hypothesis that infarction is a hallmark of systemic coronary disease activity. Changes might vary according to the "maturation" stage of an atheroma, and maximal expression would be at the level of the offending plaque. Shrinkage, thrombolysis, or vascular remodeling would determine the residual plaque morphology.

Analysis of Variance↗