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

To evaluate the relationship among supraventricular and ventricular arrhythmias with blood pressure and heart rate (HR) values, we studied 2 groups of 20 hypertensive men with (group I) and without (group II) left ventricular hypertrophy. Ambulatory electrocardiographic tracings were recorded continuously, together with ambulatory arterial pressure. Systolic (SBP) and diastolic (DBP) blood pressure values measured over 24 h showed no difference between the two groups, but we found greater variability in SBP in group I. The incidence of ventricular and supraventricular arrhythmias was significantly higher in patients of group I; moreover, we found a strong correlation between the incidence of ventricular extrasystoles (VPCs) and SBP, DBP, and HR values in group I, whereas in group II the incidence of supraventricular extrasystoles (APCs) was higher during peaks of SBP and HR values. The relationship between APCs and SBP observed in group II may be attributable to the pressure stimulus on a normal atrium, and the significant correlation between VPCs and SBP, DBP, and HR values may be due to episodes of subendocardial ischemia or to the influence of adrenergic stimulation on previously compromised myocardial tissue.
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PMID:Cardiac arrhythmias as correlated with the circadian rhythm of arterial pressure in hypertensive subjects with and without left ventricular hypertrophy. 214 53

Left ventricular hypertrophy has been identified as a powerful risk factor for sudden death and for general cardiovascular morbidity and mortality. Left ventricular hypertrophy has been documented as giving rise to ventricular ectopy, even in the absence of myocardial ischemia. Mechanisms of ectopic impulse generation in left ventricular hypertrophy are multifactorial and involve enlarged myocytes, focal areas of fibrosis, and subendocardial ischemia, as well as medial hypertrophy of the coronary arteries impeding homogeneous impulse propagation throughout the myocardium. Left ventricular hypertrophy can be reduced by specific antihypertensive therapy although not all antihypertensive agents are equally effective. A reduction of left ventricular hypertrophy with calcium antagonists, and possibly also with beta-blockers, has been shown to diminish ventricular arrhythmias. Whether or not such a reduction of left ventricular hypertrophy and suppression of ventricular ectopy will improve their unfavorable prognosis remains to be determined.
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PMID:Left ventricular hypertrophy, arterial hypertension and sudden death. 215 34

Spectral analysis of electrocardiographic signals has been proposed as a tool to detect features reflecting cardiac diseases, such as ventricular hypertrophy, myocardial infarction, and a predisposition to sustained ventricular tachycardia. The lack of a theoretical basis to address this question prompted the authors to undertake a simulation study using a bidomain volume conductor model of a strip of cardiac tissue, combined with Fourier analysis, and electrograms recorded from an isolated right atrial canine preparation. In the crista terminalis, the bandwidth of the normal electrogram was 840 +/- 200 Hz (mean +/- SD) during longitudinal propagation and 660 +/- 370 Hz during transverse propagation. During premature stimulation, signal bandwidth and propagation velocity increase with the coupling interval. In the model, a linear combination of Vmax and propagation velocity values allows simulation of the various features of premature excitation. Vmax is the major determinant of the high-frequency content of the signal. An important decrease in the high-frequency content of electrograms occurs when the recording electrode is moved away from the preparation or the simulation model; at distances larger than 1-5 mm, the bandwidth levels off to a value of 50-120 Hz. Partial blockade of axial current flow in the direction of propagation due to microscopic discontinuities and variable activation delays at these discontinuities may be the cause of fragmented activity in necrotic myocardium, which is associated with a reduced bandwidth. Thus, short- and long-term effects of ischemia followed by infarction, such as decreased propagation velocity, decreased action potential upstroke, and fragmentation, tend to decrease the electrocardiographic bandwidth.
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PMID:Simulation and experimental studies of the factors influencing the frequency spectrum of cardiac extracellular waveforms. 234 14

Hearts with advanced pressure-overload hypertrophy from systemic hypertension have been shown to have an increased susceptibility to the development of diastolic dysfunction in response to tissue hypoxia and ischemia. It is not known if this propensity to develop diastolic dysfunction in response to ischemia is dependent on the presence of a substantial increase in left ventricular mass, or alternatively, is characteristic of hearts subjected to mild chronic hypertension early in the development of cardiac hypertrophy. We tested the hypothesis that systemic hypertension associated with mild left ventricular hypertrophy increases the susceptibility to the development of diastolic dysfunction in response to demand ischemia. The effects of demand ischemia (6 minutes) were studied in hearts from New Zealand white rabbits with chronic systemic hypertension produced by the one-kidney, one-wrap method (n = 15) and compared with age-matched, sham-operated control rabbits (n = 11) with similar left ventricular mass (5.4 +/- 0.2 vs. 5.4 +/- 0.3 g, respectively). The hearts were studied using an isolated, isovolumic (balloon in left ventricle) preparation with absent pericardium that was perfused with fresh whole blood. At baseline, coronary perfusion pressure was 100 mm Hg with comparable coronary flow per gram left ventricular weight; the hearts were paced at a physiological rate of 3 Hz, and the left ventricular balloon volume was adjusted to achieve a left ventricular end-diastolic pressure of 15 mm Hg in both groups. Left ventricular balloon volume was similar in both groups and volume was thereafter held constant. At baseline, left ventricular systolic pressure (114 +/- 4 vs. 95 +/- 3 mm Hg, p less than 0.001) and developed pressure (18.9 +/- 1.2 vs. 15.1 +/- 0.9 mm Hg/g, p less than 0.05) were higher in the hearts from the hypertensive group in comparison with the control group. During the first minute of global ischemia produced by reducing coronary perfusion pressure from 100 to 20 mm Hg, there was an immediate fall in left ventricular systolic pressure in both groups without an increase in diastolic pressure. In response to the superimposition of pacing tachycardia (heart rate, 6 Hz) during the remaining 5 minutes of the period of ischemia, left ventricular developed pressure was comparable. However, isovolumic left ventricular end-diastolic pressure (measured during long diastoles obtained with transient cessation of pacing) rose to a significantly higher level in the hearts from hypertensive rabbits than in those from the control rabbits (29 +/- 3 vs. 18 +/- 2 mm Hg, p less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Influence of hypertension with minimal hypertrophy on diastolic function during demand ischemia. 252 16

It has been suggested that complex ventricular arrhythmias commonly occur in hypertensive patients with left ventricular hypertrophy. We have previously demonstrated that coronary artery ligation in anesthetized spontaneously hypertensive rats (SHR) and their normotensive controls (WKY) resulted in a significantly increased incidence and duration of ventricular fibrillation in SHR compared with WKY. The object of the present study was to characterize the structural and electrophysiological abnormalities in hypertrophied hearts, associated with the occurrence of arrhythmias. We used a double tissue bath in which a ventricular strip was exposed simultaneously to normal and to altered conditions (low pH, hypoxia and high potassium). Electrical activity recorded using standard micro-electrode techniques showed the occurrence of arrhythmias in all preparations and the development of major alterations in conduction (a conduction block appeared at 11 +/- 1 mn in SHR vs 16 +/- 1 mn in WKY, p less than 0.05), and maximal upstroke velocity (Vmax values before and 3 mn after the beginning of ischemia were 229 +/- 12 to 46 +/- 7 v/s for the SHR and 227 +/- 10 to 106 +/- 12 v/s for the WKY; p less than 0.001). These changes were associated in hypertrophied ventricles with a marked sub-endocardial collagen fibrosis as estimated by the use of automated image analysis (subendocardial collagen density = 4.39 +/- 0.34 p. 100 in SHR vs 1.66 +/- 0.15 p. 100 in WKY; p less than 0.001). Action potential duration measured using conventional glass micro-electrodes in a single chamber tissue bath revealed a highly significant difference (p less than 0.001) in APD 90 p. 100 of papillary muscles between SHR (114.7 +/- 2.8 ms) and WKY (76.9 +/- 1.7 ms). The addition of tetra-ethylammonium to block potassium channels induced triggered activity arising from early afterdepolarizations only in muscles hypertrophied SHR hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hypertensive myocardial hypertrophy and rhythm disorders: 2 possible origins]. 253 Sep 53

While calcium entry blockers have a beneficial influence on the postischemic recovery of the nonhypertrophied heart, their influence on the hypertrophied heart has not been determined. The aim of this study was to assess postischemic recovery of myocardial performance and energy metabolites in rat hearts with left ventricular hypertrophy pretreated either chronically or acutely with verapamil. Left ventricular hypertrophy was induced by suprarenal constriction of the abdominal aorta. Hemodynamics and phosphorus 31 magnetic resonance spectra were monitored simultaneously in the isolated hearts during control perfusion, after 30 minutes of global ischemia, and after 30 minutes of reperfusion. All hypertrophied hearts had significantly higher rate-pressure products than normal hearts. Compared with normal hearts, oxygen consumption was significantly lower in all hypertrophied hearts, especially untreated hypertrophied hearts. Also, before ischemia all normal or hypertrophied hearts (treated or untreated) began with comparable phosphorylation potentials (i.e., the supply of energy was not significantly different). Postischemic recovery was not related to energy supply-oxygen demand before onset of ischemia. Furthermore, it was not related to energy levels or intracellular pH during ischemia. For postischemic recovery, the rate-pressure product was 40 +/- 5% in the hypertrophied heart, 83 +/- 5% in the normal, 100 +/- 3% in the hypertrophied heart chronically treated with verapamil, and 82 +/- 5% in the hypertrophied heart acutely treated with verapamil. The degree of recovery was related to coronary flow both before and after ischemia. The latter is important for flushing deleterious metabolites and ions from the interstitial space as well as for delivery of oxygen and substrate to the myocardium.
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PMID:Verapamil preserves myocardial performance and energy metabolism in left ventricular hypertrophy following ischemia and reperfusion. Phosphorus 31 magnetic resonance spectroscopy study. 253 75

Ischemia, followed by reperfusion and restoration of oxygen to tissues, generates hydrogen peroxide which in turn generates injurious free radicals, particularly hydroxyl. Chronic hypoxia may also result in liberation of free radicals. In rats, chronic hypoxia causes pulmonary hypertension, associated with structural remodelling of pulmonary arteries, polycythemia, and vasoconstriction. We studied in rats the effects of dimethylthiourea (DMTU), a hydroxyl and hydrogen peroxide scavenger, on acute hypoxic vasoconstriction, and on the arterial structure and development of polycythemia after chronic hypoxia (FIO2 0.10 for 10 days, daily DMTU). DMTU did not affect acute vasoconstriction nor polycythemia. It significantly reduced muscularization of alveolar wall and alveolar duct arteries, medial thickening of alveolar wall and preacinar arteries, and right ventricular hypertrophy, suggesting reduction of pulmonary hypertension. However, DMTU caused marked growth retardation in both control and hypoxic rats, an effect not previously described. In other rats a similar degree of growth retardation due to reduced food intake failed to prevent the effects of hypoxia, suggesting that DMTU's effect is not through this mechanism. The results of this study support but do not confirm the hypothesis that free radicals may have a role in the pathogenesis of the arterial structural changes in the microcirculation contributing to chronic hypoxic pulmonary hypertension. However, in view of DMTU's effects on growth, definitive testing of the hypothesis will not be possible until other, less toxic, chronic hydroxyl scavengers become available.
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PMID:Effects of dimethylthiourea on chronic hypoxia-induced pulmonary arterial remodelling and ventricular hypertrophy in rats. 253 91

The introduction, more than twenty years ago, of beta-blockers in the treatment of arterial hypertension, represented a significant advance. With these medications, many hypertensive patients are effectively under control and malignant hypertension is practically inexistent. Today, the treatment of hypertension is markedly improved with the development of new, active medications, while the beta-blockers family has markedly evolved. The role of beta-blockers in the treatment of hypertension, must therefore be re-evaluated according to their properties as compared to those of other classes of antihypertensive medications. Indeed, there are standard contraindications to he use of beta-blockers, sometimes resulting in adverse reactions, either clinical (fatigue, sexual disorders, vasomotor syndromes)--much less frequent with the new molecules--or biological (especially serum lipid levels), the consequences of which remains ill-defined--some beta-blockers appear practically without any harmful effect. Actually, despite these drawbacks, usually minimal, there are numerous and strong arguments in favor of the use of beta-blockers in the treatment of hypertension: 1) their significant follow-up in the treatment of hypertension; this is a well-known argument; 2) their effectiveness in hypertension, as a single drug and single daily dose; 3) their cost, which is lower than that of new anti-hypertensive medications; 4) their cardio-protective role, demonstrated by experimental data (myocardial protection and anti-arrhythmic effect in experimental ischemia), and clinical data (improvement of left ventricular hypertrophy, control of blood pressure increase during exertion and stress, secondary prevention after myocardial infarction).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of beta-blockers in the treatment of arterial hypertension]. 256

The prognosis for patients with non-Q-wave myocardial infarction (MI) remains controversial, although a number of studies have shown a less favorable outlook after hospital discharge for patients with non-Q-wave than for those with Q-wave infarction. Numerous management strategies are available to the clinician, many of which involve an interventional strategy (myocardial revascularization with coronary bypass surgery or angioplasty) or a more conservative approach which emphasizes secondary prevention with medical therapy. This review summarizes the role of identifying risk variables in patients with non-Q-wave MI and their importance to clinical decision making. Based on data obtained from the Diltiazem Reinfarction Study (DRS), it has been shown that 20% of patients experience one or more episodes of spontaneous postinfarction angina which is associated with a significant increased (33%) 2-week mortality and an appreciable fivefold increased incidence of early reinfarction compared to patients without early recurrent ischemia. Similar findings have been observed in this same cohort of patients who were followed for one year, in that there was twofold higher incidence of death and late reinfarction at one year of follow-up. Other risk factors also appear to be important determinants of adverse long-term outcome after non-Q-wave MI and include persistent ST segment depression on serial electrocardiograms, congestive heart failure, and left ventricular hypertrophy. Medical therapy employed for secondary prophylaxis after non-Q-wave MI has failed to show a convincing therapeutic rationale for beta blocker administration. In contrast, diltiazem has been shown to influence the early and late outcome following non-Q-wave MI favorably.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Strategies for managing the patient with acute non-Q-wave myocardial infarction. 257 20

Abnormalities of the posterior cardiac wall are often small and obscured by electrical activity of the anterior wall of the left ventricle or by right ventricular hypertrophy. The posterior wall is hidden from the precordial leads by the anterior wall, and electrodes placed on the back are of little use because of their distance from the heart and of the intervening high-resistivity lungs. In contrast to the body surface, the esophagus provides a unique perspective of the posterior aspects of the heart at close range. The authors employed a noninvasive approach to produce cardiac stress and simultaneously record posterior cardiac electrical activity via the esophagus. A new esophageal electrode and instrumentation were developed for acquiring a high-quality esophageal electrocardiogram (ECG) during transesophageal atrial pacing stress. They present their technique for combining stress testing and computer analysis of ST-segment changes in the esophageal ECG as well as preliminary results from one normal subject and one patient with known posteroinferior ischemia.
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PMID:A system for simultaneous esophageal atrial pacing and ventricular recording in computer analysis of posterior ischemia. 261 9


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