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)

Reduction in pH is known to decrease O2 affinity (Bohr effect) and increase the rate of O2 release from blood. It provides a potential mechanism for increasing O2 transport to the myocardium. Fifteen patients with refractory, chronic angina were studied by treadmill exercise tolerance tests and whole blood-oxygen release rate measurements before and 4 days after beginning treatment with oral acetazolamide (10 to 20 mg/kg body weight). Positive treadmill exercise test or myocardial necrosis was present in each case. There was a correlation between an increased O2 release rate from blood and relief of symptoms. The major side effect in 2 patients with pathologic fatigue believed to result from acidosis. Of the 7 patients who obtained relief from angina, in each there was a 27% increase in the rate of release of O2 from their whole blood. Seven patients did not obtain relief; they showed no change in the rate of release. In the 4 patients who became worse the rate of deoxygenation decreased by 22%. All changes in deoxygenation rate coincided with the clinical findings. The treatment of ischemic heart disease with acetazolamide or other acidifying agents should not, however, be attempted until further investigation establishes their clinical value.
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PMID:Effect of acidosis on patients with myocardial ischemia. 24 34

Among 2485 patients with cardiovascular pathology observed by the authors in the course of 3 years, 8 patients displayed the mitral valve prolapsus syndrome due to the presence of a late systolic murmur or extratone (nonejection systolic click). In 5 patients the diagnosis was supported by echocardiography. In 3 patients, aged 58 to 77 years different forms of the ischaemic heart disease were diagnosed. In the remaining 5 younger patients (24 to 35 years) the etiology of the mitral valve prolapsus syndrome was not established. Their clinical manifestations consisted in complaints of cardiac pains not connected with physical exercises, extrasystole, fatigue, neurotic behaviour.
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PMID:[Mitral valve prolapse syndrome]. 101 10

Conventional formulations of metoprolol have become well established in cardiovascular medicine and are particularly useful in the management of hypertension and ischaemic heart disease. Recently developed controlled release metoprolol delivery systems (metoprolol CR/ZOK and metoprolol OROS) were designed to overcome the drug delivery problems of matrix-based sustained release forms by releasing the drug at a relatively constant rate over a 24-hour period, and thus producing sustained and consistent metoprolol plasma concentrations and beta 1-blockade while retaining the convenience of once daily administration. Clinically and statistically significant reductions in blood pressure have been observed with metoprolol CR/ZOK and metoprolol OROS 24 hours after administration in mildly or moderately hypertensive patients. Studies in patients with mild to moderate hypertension have demonstrated that a similar or higher percentage of patients achieved a goal response with metoprolol CR/ZOK compared with matrix-based sustained release formulations of metoprolol, or conventional atenolol or bisoprolol, while metoprolol OROS achieved an equal or greater response rate compared with conventional or matrix-based sustained release metoprolol preparations. In patients with stable effort angina pectoris, once daily administration of metoprolol CR/ZOK provided at least equal antianginal efficacy as conventional metoprolol in divided doses, while metoprolol OROS reduced the mean number of anginal attacks by the same margin as atenolol. Controlled release metoprolol formulations have been well tolerated in clinical trials. Metoprolol CR/ZOK was associated with a similar or lesser degree of adverse effects related to the central nervous system compared with atenolol or long acting propranolol. Metoprolol CR/ZOK also demonstrated less pronounced beta 2-mediated bronchoconstrictor effects than atenolol in asthmatics, and less general fatigue and leg fatigue in healthy subjects. Metoprolol OROS produced less pronounced bronchoconstrictor effects than atenolol, matrix-based sustained release metoprolol or long acting propranolol in patients with asthma or obstructive airways disease, and healthy volunteers. These results are presumably due to the beta 1-selectivity of metoprolol in addition to the relatively low plasma concentrations maintained by metoprolol CR/ZOK and metoprolol OROS, and the avoidance of high peak plasma concentrations with these agents. Despite the relative safety of the controlled release forms of metoprolol, the use of all beta-adrenoceptor antagonists should be avoided in patients with a history of bronchospasm. Thus, controlled release metoprolol formulations offer the potential to maximise the confirmed benefits of this agent in the management of hypertension and angina, by maintaining clinically effective plasma concentrations within a narrow therapeutic range over a 24-hour dose interval.
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PMID:Controlled release metoprolol formulations. A review of their pharmacodynamic and pharmacokinetic properties, and therapeutic use in hypertension and ischaemic heart disease. 137 20

The adequate treatment of a disease syndrome is dependent upon a clear definition of the symptomatic, pathological, physiological and prognostic targets against which therapy is to be deployed. The syndromes of ischaemic heart disease, including angina pectoris, are complex in origin, pathology, pathophysiology and natural history, and a complete clinical profile is difficult, if not impossible, to achieve in individual patients. The prime goals of pharmacotherapy in ischaemic heart disease are easy to define, but difficult to accomplish in practice. Relief of pain, breathlessness and fatigue are the prime clinical targets for pharmacotherapy. In view of their sinister significance, the electrophysiological indications of myocardial ischaemia, whether symptomatic or silent, are also crucial targets towards which therapy must be directed. Ischaemic heart disease is accompanied by a wide variety of regional and global abnormalities of myocardial contractile function associated with widespread reflex stimulation of the peripheral vascular system and neuroendocrine systems. Primarily, drug therapy must be directed at correction of these pathophysiological components of the syndrome. Longer term but no less essential goals in the treatment of ischaemic heart disease are the prevention of the clinical sequelae of the syndrome and its progression. A natural sequel of coronary artery obstructive disease is successive thrombotic events and loss of myocardium. Calcium antagonists, by preventing the increase in myocardial cytosolic calcium during acute ischaemic episodes, defer cell necrosis; in this respect, they are unique among currently available antianginal drugs. With regard to progression, the prime pathological cause of ischaemic heart disease is coronary atheroma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapeutic targets in ischaemic heart disease. 137 82

Exercise performance data, circulatory function and respiratory and leg muscle quality, expressed as muscle fiber composition, are reviewed and together with our own data discussed as possible limiting factors for physical performance in chronic obstructive pulmonary disease (COPD). COPD is regarded as synonymous with reduced physical performance, exaggerated breathlessness or dyspnea, muscle hypotrophy and/or wasting and, frequently, malnutrition. Impaired right ventricular circulatory function seems to be essential. The observed preponderance of fast twitch (FT), 'glycogenolytic' and capillary-poor muscle fiber type in the investigated muscles might reflect endowment, a 'hypoxic vasoconstriction'-related downregulation of the other main fiber type: the slow twitch (ST), capillary-rich, fatigue-resistant fiber, and/or selective muscle trauma to ST fibers. Ischemic heart disease (IHD) patients demonstrate a similar fiber type pattern in leg muscles. Both COPD and IHD patients have low leg muscle and plasma deposits of antioxidants such as coenzyme Q10 (CoQ10) and alpha-tocopherol. This could reflect a depressed resistance to radical induced cell trauma and/or malnutrition. The magnitude of the antioxidant reduction is less pronounced in patients rich in FT fibers indicating a ST fiber-related susceptibility to trauma. Treatment of other muscle disorders including heart muscle with, e.g., CoQ10 improves performance due to a causative enhanced antioxidant potential, reduced catabolism and/or an upregulated muscle anabolism, increased mitochondrial volume/function, etc. Such data are lacking in COPD.
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PMID:Exercise-limiting factors in respiratory distress. 151 68

Safety information was pooled from 4,859 patients, mainly treated in controlled clinical trials with a dispersible tablet of sumatriptan or by a subcutaneous injection, and from 1,164 patients who received placebo by these routes. Safety monitoring involved collection of all adverse events, regardless of their relationship to treatment, and included routine laboratory screening tests and some special investigations. Individuals experienced several groups of symptoms that might be considered to be features of migraine itself or of the post-migraine period or due to treatment. The commonest complaints were an unpleasant taste or pain on injection. After oral sumatriptan (100-300 mg), some events (nausea, malaise) were characteristic of migraine and others (fatigue, sedation, weakness) were characteristic of the recovery period. With subcutaneous sumatriptan (4-8 mg) similar events were observed, but certain distinctive symptoms variously described as heaviness, pressure sensation, tingling, feelings of heat or warmth, were more common and affected various parts of the body. Their early onset and transient nature suggests some pharmacological mechanism, as yet not identified. Despite the mixed picture of symptoms recorded after treatment, they were not serious, they were transient and they were accepted by patients. Close patient monitoring allowed detailed evaluation of any possible cardiovascular side-effects as seen with other anti-migraine agents, particularly ergotamine. The evidence is reassuring but, since experience in patients with symptomatic ischaemic heart disease is limited, it is recommended that they should initially be treated with sumatriptan under medical supervision for their first two or three attacks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The safety and tolerability of sumatriptan: an overview. 165 42

Assessment of functional capacity, of ability and disability among patients with cardiovascular disease raises a number of problems and issues for which there are currently only imperfect or incomplete answers. Emphasis must be placed on the lack of predictable relationship of anatomic abnormality and functional abnormality. For example, the percentage obstruction of the coronary artery documents the anatomic extent of the disease, rather than the limitation of functional capacity; the same lack of predictive value characterizes the decrease in resting ventricular ejection fraction. The response to a challenge of activity or exertion currently appears to offer the optimal method of assessing functional capacity for work, although a brief continuous exercise test may not be the optimal exercise protocol by which to evaluate endurance. As an example, in our laboratory, comparing a low-level continuous exercise test protocol with one with an intermittent exercise design (i.e., periods of exercise alternating with periods at rest), patients typically can perform at least one additional stage of exercise on the discontinuous or intermittent test protocol. This occurred without significant differences in the final heart rate, blood pressure, or rate-pressure product, probably because most patients so tested were limited not by myocardial ischemia but by musculoskeletal problems, fatigue, or dyspnea (8). An unmet need is a comparison of exercise test protocols for the assessment of functional capacity, possibly the development of new test protocols for patients with limited functional capacity, and the evaluation of the relationship of these test data to eight hours of occupational activity in the workplace setting. It appears logical that a diagnostic exercise test should differ from one designed to determine functional capacity, but the results of a variety of exercise test protocols should be compared with the actual physical activity able to be performed in the workplace, as well as with reported symptoms. It should be defined whether testing is to be performed on optimal medical therapy, which I believe should be the case; or whether the technique used for diagnostic exercise testing, that of the minimal medication possible, is to be employed. Next, the time after surgical intervention or following a prolonged hospitalization at which to test should be delineated in that the deconditioning effect of immobilization may substantially decrease effort tolerance, unrelated to the severity of the underlying cardiovascular disease. Finally, should exercise rehabilitation be recommended or required before testing for cardiovascular impairment; major improvement in functional capacity has occurred in previously sedentary patients with a variety of cardiovascular diseases, including those with important manifestations of myocardial ischemia and ventricular dysfunction.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Ability, disability, and the functional capacity of patients with cardiovascular disease. 185 30

To compare cardiorespiratory responses to standing arm ergometry and treadmill exercise, two graded exercise stress tests were performed in 30 patients with ischemic heart disease (IHD). Cardiac catheterization and expired gas analyses were also done. Standing arm ergometry was discontinued because of arm fatigue in 15 (50%) patients, whereas treadmill exercise was stopped due to leg fatigue in 8 (27%) patients. Maximal increase in rate-pressure product and oxygen uptake, and magnitude of ST-segment depression during standing arm ergometry were significantly smaller (p less than 0.01, p less than 0.01 and p less than 0.05, respectively) than those during treadmill exercise. Furthermore correlations of maximal change in rate-pressure product, oxygen uptake and extent of ST-segment depression were not close between the two exercise tests (r = 0.76, r = 0.67 and r = 0.54, respectively). Our results indicate that the ability to detect IHD with standing arm ergometry is lower than that with treadmill exercise and that it is not possible to predict accurately one's capacity for arm exercise from the treadmill exercise test.
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PMID:Cardiorespiratory responses to standing arm ergometry in patients with ischemic heart disease. Comparison with the results of treadmill exercise. 195 14

The long term effects of treatment with xamoterol in 14 patients aged 44-73 with mild to moderate heart failure as a result of ischaemic heart disease are reported. After 18 months' treatment with xamoterol, patients were assessed in a randomised double blind crossover comparison of xamoterol (200 mg twice a day) and placebo, each given for one month. Compared with placebo, xamoterol significantly increased exercise duration and work done on a bicycle ergometer and reduced the maximum exercise heart rate. Assessment of symptoms and activities at 12 months by visual analogue and Likert scales showed a trend towards the relief of symptoms of breathlessness and tiredness and an improvement in activity. There was an improvement in the clinical signs of heart failure and no haemodynamic deterioration over a 12 month period as assessed by ejection fraction. The improvement in exercise tolerance, symptoms, and activities was sustained for 18 months without side effects or development of tolerance.
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PMID:Ischaemic left ventricular failure: evidence of sustained benefit after 18 months' treatment with xamoterol. 197 39

Impaired diastolic function of the hypertrophied and stiffened left ventricle is a characteristic feature of hypertrophic cardiomyopathy (Figure 1). Altered left ventricular filling dynamics and reduced left ventricular distensibility or increased left ventricular diastolic chamber stiffness are associated with reduced left ventricular stroke volume, increased left ventricular filling pressures and compressive effects on the coronary microcirculation. These factors contribute importantly to the clinical presentation of many patients, including symptoms of fatigue, dyspnea and angina pectoris. Reduced distensibility results both from factors determining the passive elastic properties of the ventricular chamber (including severity of hypertrophy, fibrosis and cellular disarray) and from factors influencing the rate and extent of active left ventricular relaxation (Figure 2). The factors contributing to impaired relaxation in hypertrophic cardiomyopathy are mediated via either inactivation dependent or load-dependent mechanisms. In laboratory animals, compromise of myocardial inactivation results in a persistent increase in intracellular calcium concentration and in prolonged interaction of the contractile proteins. Additionally, there is evidence for an increased number of active receptors for calcium antagonists and, lastly, for myocardial ischemia (Figure 3). Load-dependent mechanisms include diminished wall tension at the opening of the mitral valve, changes in afterload, contractility and coronary flow. Other factors are nonuniform and asynchronous regional ventricular function due to differing increases in thickness of the ventricular walls and ischemia (Figure 4). Calcium channel blockers exert a favorable influence on left ventricular relaxation and filling (Figure 5); verapamil and diltiazem are preferable to nifedipine. Verapamil increases left ventricular stroke volume without an increase in the end-diastolic pressure (Figure 6), reduces regional asynchrony if present, and leads to a more homogeneous regional diastolic filling (Figure 4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular diastolic function in hypertrophic cardiomyopathy. 202 81


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