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This review summarizes selected topics discussed at one of the major congress events in cardiovascular medicine in Great Britain in 1989. The congress was attended during its five days duration by 800 participants from nearly 40 countries. The scientific programme, consisting of invited state-of-art lectures, was divided into following basic topics: coronary heart disease including risk and prevention, arhythmias, hypertension, heart failure, structural heart disease, cardiac imaging and costs-effectiveness of cardiology. The aim of the review is to bring nearer the creative atmosphere and the very advanced postgraduate level of this cardiologic meeting. Due to the actual medico-social importance of current strategies in management of ischemic heart disease and malignant arrhythmias in Czechoslovakia, special interest is devoted to these problems. Based on congress lectures an overview of the atherosclerotic plaque pathology and resulting therapeutic and prognostic implications for the management of unstable angina and myocardial infarction is given. Selected aspects of thrombolytic therapy and its impact on coronary vessel wall and myocardium are discussed, too. Some contemporary problems and updated concepts of both drug and intervention treatment of malignant ventricular arrhythmias are highlighted in a more extensive way, confronting congress speakers and recent publications.
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PMID:[Cardiology '89. Present trends in cardiovascular medicine at the Congress of Cardiology '89 in London April 1989]. 233 60

Organic nitrates are well established in the treatment of a wide variety of cardiovascular disorders, most notably angina pectoris and congestive heart failure. However, attenuation of, or tolerance to, haemodynamic and anti-ischaemic effects may occur with all long-acting nitrate formulations. In the majority of patients continuous administration of long acting nitrates tends to promote the development of attenuation, while intermittent administration avoids it. Likewise, higher-doses appear to induce attenuation to a greater degree than lower doses. Attenuation of haemodynamic effects and exercise tolerance in heart failure patients, and of clinical end-points in angina patients, appears to be less than attenuation of exercise testing end-points in angina patients. While the use of intermittent therapy avoids the development of attenuation, it may expose the patient to an as yet undefined risk of silent and/or symptomatic anginal episodes occurring during the nitrate-free interval. Likewise, the role of concomitant therapy in avoiding this potential risk remains to be defined. Means of avoiding attenuation may include the coadministration of sulfhydryl donors such as N-acetylcysteine. Alternatively, angiotension-converting enzyme (ACE) inhibitors such as captopril may block renin-angiotensin system-induced reflex sympathetic stimulation. Attenuation may occur to a greater or lesser degree in individual patients. The proportion of attenuators vs non-attenuators remains to be defined, as does a means of identifying such patients prospectively by clinical and/or laboratory parameters. Conflicting results among smaller studies may reflect variable proportions of attenuators vs non-attenuators. However, conflicting results among larger studies may reflect differences in patient selection criteria, such as selecting patients with positive and reproducible stress tests and little in the way of spontaneously occurring angina versus selecting patients with positive but variable stress tests and frequent episodes of spontaneously induced angina. The former group may reflect pure fixed coronary artery disease with little in the way of vasospasm, or change in vasomotor tone, while the latter group may reflect greater variability in vasomotor tone and/or more in the way of plaque instability. The clinical efficacy of long acting nitrates might therefore be expected to be greatest in those patients with larger numbers of spontaneously occurring angina episodes. Recent data suggest that nitrates may have important direct effects on coronary vessels including dilating eccentric coronary stenoses, dilating intercoronary collateral channels and having greater dilating effects on more diseased segments as opposed to less diseased coronary segments.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nitrate tolerance. A review of the evidence. 266 Nov 97

The antithrombotic approach to patients with acute myocardial infarction in the prevention of venous, left ventricular and coronary artery thromboembolic events should be based on an understanding of pathogenesis and risk. Coronary thrombotic events involve conditions of high shear rate present in areas of vessel stenosis or disrupted atherosclerotic plaque, which lead to activation of both platelets and the coagulation system, and are best prevented by platelet inhibitors alone or in combination with an anticoagulant. However, thromboembolism that originates in the venous system or cardiac chambers is related to situations of blood stasis and low shear rate, which predominantly result in clotting activation and fibrin-thrombus formation and are best approached with anticoagulant therapy. For prevention of venous thrombosis and pulmonary embolism, early mobilization is essential and should be supplemented by low-dose heparin in patients at high risk, including the elderly and those with large infarcts, heart failure or previous thromboembolic events. For prevention of left ventricular mural thrombosis and systemic embolism, high-dose heparinization is indicated in patients with large infarcts, particularly in the anterior location and in those with heart failure. Subsequently, warfarin therapy should be considered for patients at high embolic risk, including those with echocardiographic evidence of mobile and protruding thrombi, severe left ventricular dysfunction or prior emboli. In patients with acute infarction, aspirin is recommended for preventing coronary reocclusion and reinfarction. Although anticoagulants may also be of benefit for this purpose, their use is still controversial.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antithrombotic therapy in acute myocardial infarction: prevention of venous, left ventricular and coronary artery thromboembolism. 266 69

A case of acute pulmonary edema without cardiac failure, infectious or toxic cause, revealing a Multiple Sclerosis (M.S.), one case of bradycardia during a bout in a known M.S. and one case of orthostatic hypotension without change of cardiac frequency, during a bout of a known M.S. are reported. The common point of these 3 cases is that during their autonomic failure, there were disorders pointing to the medulla oblongata: swallowing difficulties, rotatory nystagmus, vestibulo-cerebellar syndrome, sensory and motor defect of upper limbs. A plaque of M.S. in the medulla oblongata, particularly near the tractus solitarius could explain these cardio-pulmonary abnormalities unusual in M.S.
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PMID:[Cardio-respiratory anomalies in disseminated sclerosis]. 304 35

A 78 year old man underwent aortic valve replacement because of acute aortic regurgitation and intractable heart failure. At operation the intact commissure between the left and right coronary cusps of a grossly normal aortic valve was found to have separated from the aortic wall. Histopathological examination of the surgical specimen showed that the site of separation was an atheromatous plaque. This is believed to be the first report of this feature.
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PMID:Dehiscence of an atheromatous plaque at an aortic valve commissure: an unusual cause of acute aortic regurgitation. 337 Jan 89

Sudden cardiac death, most often due to ventricular fibrillation, is caused by three vessel coronary disease in over 90% of the cases. At autopsy acute coronary thrombosis superimposed on an arteriosclerotic plaque is often found. However, a terminal myocardial ischemia can also develop without coronary thrombosis. In these cases platelet thrombi or coronary spasm may be the cause of ventricular fibrillation. In approximately one fourth of all patients with coronary disease sudden death is the first manifestation of the patient's illness. After myocardial infarction a high risk patient group can be detected by non-invasive methods: patients with cardiac failure, high enzyme values, a positive exercise-ECG and malignant ventricular arrhythmias three weeks after myocardial infarction have a significantly higher mortality in the following 12 months than patients without these complications. In this group of patients prevention of sudden death should be tried by an aggressive management of myocardial ischemia, heart failure and ventricular arrhythmias.
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PMID:[Sudden cardiac death]. 399 33

Coronary artery disease is described by its extreme presentations. At one end we see the slowly growing fibrous plaque gradually occluding the artery. Collaterals develop and confine the loss of myocardium to the inner layer of the left ventricle. At the other end of the spectrum we see the rupture of a soft plaque. Blood breaking in an atheroma occludes a coronary artery suddenly. There is no time to develop collaterals. The myocardial infarction corresponds in its size to the perfusion-area of the occluded artery. Transmural infarctions lead to rupture of the free wall, ventricular septum or papillary muscle. The coronary morphology of our patients suffering from coronary heart disease lies between these two extremes. However, many patients die suddenly due to arrhythmia a long time before the loss of myocardium disturbs left ventricular pump function so severely that lethal heart failure may develop.
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PMID:[Anatomic-pathological bases of coronary heart disease]. 748 30

Aim of recent experimental and clinical studies has been to evaluate the important role of the renin-angiotensin system in the development of cardiac hypertrophy, of vascular hypertrophy and of left ventricular fibrosis and remodelling in essential hypertension and ischemic heart disease. It has been suggested that ACE-inhibitors are the class of antihypertensive drugs more effective in reducing left ventricular hypertrophy (LVH) in hypertensive patients. The possible mechanisms are, beyond the decrease in blood pressure, the possibility of interfering not only with the renin-angiotensin system activity, but also with the sympathetic nervous system activity as well as with aortic distensibility, all factors that can influence the development of LVH. Vascular changes in essential hypertension are complex and depend not only on the severity of blood pressure levels, but are related to diameter and structure of the vessels and to the presence of other atherosclerosis risk factors. ACE-inhibitors are effective in inducing the regression of structural changes in resistance arterioles and furthermore can increase arterial compliance in large arteries; new studies are undergoing in order to assess the effects of these drugs on atherosclerotic plaque progression/regression. The results of large clinical trials have shown the efficacy of ACE-inhibitors in the treatment of heart failure, in addition, after it has been demonstrated that ACE-inhibitors can influence the structural remodelling process after myocardial infarction, their use has been extended to patients with ischaemic heart disease.
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PMID:[ACE-inhibitors and cardiovascular protection]. 763 57

Coronary heart disease (CHD) is the most common cause of death in Western industrialized countries. CHD is more common in individuals with clustering of coronary risk factors, e.g., hypertension and blood lipid abnormalities. There is a good rationale for the use of beta-blockers for prevention of myocardial infarction (MI) in high-risk groups, as beta-blockade decreases myocardial oxygen consumption and, by decreasing turbulent blood flow patterns, reduces endothelial shear forces, thus making plaque rupture (and the ensuing thrombotic events) less likely. Clinical trial data have shown beta-blockade to be effective in the prevention of cardiovascular end points. In both younger and older hypertensive patients there is a significant reduction in the incidence of stroke and in younger hypertensive patients there is about a 15% reduction in MI. Left ventricular hypertrophy (particularly by ECG) is significantly diminished. In secondary prevention of MI there is about 15% reduction after early and 25-30% reduction after late intervention with beta-blockers given post-MI. In both stable and unstable angina, beta-blockade appears to be beneficial not only in improvement of symptoms but also in prevention of hard cardiovascular end points. There are also promising data suggesting that beta-blockade is useful in endothelial protection and atheroma prevention, and benefits patients with hypertrophic cardiomyopathy and heart failure. beta-Blockers have evolved from early nonselective agents, e.g., propranolol, to modern highly beta 1-selective agents, e.g., bisoprolol. beta 1-Blockade is the essential element that leads to the above cardiovascular benefits in addition to improving the quality of life (similar to angiotensin-converting enzyme inhibitors).
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PMID:The beta 1 hyperselectivity in beta-blocker treatment. 775 68

beta-blockers and calcium channel blockers have been evaluated extensively during the acute phase and following myocardial infarction. beta-blockers, when administered early and intravenously, reduce early mortality, reinfarction and cardiac arrests by about 16%. The reduction in mortality is likely to be due to multiple mechanisms including reductions in cardiac rupture, reinfarction and ventricular fibrillation. Recent data also suggest a reduction in intracranial haemorrhage when administered in conjunction with thrombolytic therapy. Prolonged use of beta-blockers for a year or two after myocardial infarction leads to significant reductions in total mortality, sudden deaths and reinfarction. The benefits of beta-blockers are probably mediated through a number of mechanisms, including reduction in heart rate and prevention of plaque rupture, in addition to the mechanisms stated above. Calcium channel blockers do not reduce mortality. It appears that some agents that increase heart rate (e.g. dihydropyridines) may increase the risk of death and reinfarction. On the other hand, agents that reduce heart rate (verapamil and diltiazem) appear to have a neutral effect on mortality but may reduce reinfarction rates. The benefits of beta-blockers appear to be consistent in most subgroups of patients examined, whereas the adverse effects of calcium channel blockers are most marked in those with large infarcts or heart failure. In conclusion, beta-blockers are preferable to calcium channel blockers in the acute phase and long-term after myocardial infarction.
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PMID:Effects of beta-blockers and calcium channel blockers in acute myocardial infarction. 790 43


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