Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eleven patients with short P-R intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an exprerssion of the "enhanced A-V conduction" that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamically unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies.
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PMID:Ventricular tachycardia and ventricular fibrillation in patients with short P-R intervals and narrow QRS complexes. 9 18

In patients with pump failure complicating acute infarction, vasodilating drugs, by reducing impedance to left ventricular outflow and venous return to the heart, improve cardiac performance without affecting myocardial contractility. Sodium nitroprusside currently is the vasodilator of choice in most patients with both elevated left ventricular filling pressures and reduced cardiac output. Patients with accompanying mechanical defects, such as acute mitral regurgitation or ventricular septal rupture, are particularly amenable to vasodilator therapy. Some patients may require combined therapy, with inotropic catecholamines or mechanical assistance devices together with vasodilators, in order to avoid undesirable hypotension. Side effects and toxicity are rare when patients are carefully selected and monitored. It is uncertain whether vasodilators reduce ischemia or salvage jeopardized myocardium, but they appear to improve the initial prognosis of some patients with severe pump failure. The long-term prognosis of these patients remains poor, however, and therefore a more aggressive approach to their chronic management seems warranted.
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PMID:Vasodilator therapy of pump failure complicating acute myocardial infarction. 10 78

Sixty-two autopsied hearts, with left ventricular hypertrophy (LVH) caused by mitral regurgitation (MR), aortic failure (AR), combined valvular disease (CVD), hypertension (HHD), or ischemia (IHD), and 23 control hearts with normal left ventricles were studied morphologically for analysis of modes of hypertrophy and for ECG-pathology correlation. Basic disorders modify the mode of hypertrophy; that is, elongated AR-type LV makes muscle fiber orientation in the outer layer more vertical, and globular MR-type LV makes it more horizontal than normal. High-voltage QRS correlates with hypertrophy of the outer layer which is often associated with that of the inner layer. ST depression and T changes correspond to relative deterioration of the inner and median layers, respectively.
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PMID:Histopathological study of hypertrophied myocardium of known etiologies with special reference to correlation of ECG changes. 14 36

A three-year-old girl with mitral regurgitation due to mucocutaneous lymph node syndrome (MCLS) but with normal coronary arteries was treated surgically. Although no definite pathologic lesions causing severe mitral regurgitation except for dilatation of the mitral annulus were found at operation, some minor changes implied focal ischemia of the posterior papillary muscle. A poster-medial annuloplasty was performed without significant residual regurgitation. This is the first patient successfully treated by surgery for mitral valve incompentence due to MCLS. However, additional clinical experiences will be needed to evaluate surgical treatment for this group patients.
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PMID:Mitral insufficiency secondary to mucocutaneous lymph node syndrome. A case report of successful surgical treatment. 71 29

The consequences of ischemia for the affected myocardium are highly variable. As a result, in chronic coronary heart disease there is little correlation between coronary arterial obstruction and myocardial dysfunction. Dysfunction can be permanent and related to replacement fibrosis or fixed disruption of the chain of events leading to effective contraction. Dysfunction can also be transient, as a direct consequence of acute myocardial ischemia. The mechanical lesions include generalized and localized myocardial dysfunction, mitral incompetence, and rarely, a left-to-right shunt through loss of integrity of the interventricular septum. Diagnosis per se is not difficult, but deciding on the true contribution of any given lesion to the overall symptoms and disability of the patient is. Therapy must be individually planned according to the total set of factors in each patient.
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PMID:Impaired myocardial contraction in the chronic stage. 97 42

The pathological processes underlying the symptom of mitral insufficiency appearing during the course of acute myocardial infarction are reviewed. The mitral valve apparatus can be considered as being composed of fibrous elements (the annulus fibrosus, the valve leaflet and the chordae tendineae), the left atrial endocarduim and the muscular elements (the papillary muscles together with their supporting myocardium). Since the fibrous elements are avascular, it is concluded that they are unlikely to be directly affected by ischemia. For this and other reasons dilatation of the mitral annulus is not considered a cause of incompetence. It is suggested that muscular involvement is the most likely cause of mitral incompetence during acute myocardial infarction. The syndrome of 'papillary muscle dysfunction' is therefore reviewed under the headings of (1) conditions producing abnormal spatial orientation of the muscles, (2) conditions producing abnormal or absent contraction of the muscles and (3) conditions producing improper timing of muscular contraction. Cases are illustrated which demonstrated generalized dilatation of the left ventricle, localized dilatation and both complete and imcomplete papillary muscle rupture. Mitral insufficiency under these circumstances may ensue from either improper orientation or improper functioning of the muscular elements of the mitral valve apparatus, or from both. It is also emphasized that direct involvement of the papillary muscles by the ischemic process is not necessary for incompetence to occur, and that most cases of mitral incompetence complicating the acute stage of myocardial infarction are of transient nature, resolving during the recovery phase.
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PMID:Mitral insufficiency complicating acute myocardial infarction. 114 72

Tricuspid regurgitation developed in two patients after inferior wall myocardial infarction. Neither patient had preexisting valvular heart disease or evidence of endocarditis, and neither had suffered chest trauma. Because abnormalities in right ventricular function may occur after inferior infarction, and because other known causes of tricuspid incompetence were not present, we postulate that these patients developed valvular regurgitation from dysfunction of the papillary muscle complex controlling tricuspid valve function, a mechanism similar to that proposed to explain mitral regurgitation seen with inferior wall ischemia.
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PMID:Tricuspid regurgitation following inferior myocardial infarction. 124 43

This report describes a patient who developed acute severe exacerbation of mild rheumatic mitral regurgitation caused by ischemia in the territory of a small, non-dominant circumflex coronary artery without myocardial infarction.
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PMID:Acute ischemic exacerbation of rheumatic mitral regurgitation. 147 10

The aim of this study was to evaluate the prognosis and functional outcome of mitral regurgitation caused by ischemic papillary muscle dysfunction with respect to treatment, and to determine the role of coronary angioplasty in this context. Thirty patients with severe ischemic mitral regurgitation were followed up for 33 +/- 3 months. Thirteen patients were treated medically (group I) and 17 patients underwent surgery or angioplasty (group II). The 3-year survival was 59.5% (45.6% in group I and 70.2% in group II). Angioplasty was only used in paroxysmal mitral regurgitation caused by papillary muscle ischemia. This technique resulted in spectacular immediate results in three patients with pulmonary edema caused by mitral regurgitation during myocardial ischemia. Surgical correction of mitral regurgitation should be considered without delay if angioplasty is not feasible or if the regurgitation is permanent or severe. Widening the indications of surgery or angioplasty should result in an improvement of the prognosis of these high-risk patients.
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PMID:Treatment of severe mitral regurgitation caused by ischemic papillary muscle dysfunction: indications for coronary angioplasty. 154 93

The mechanism and temporal manifestation of functional mitral regurgitation after acute myocardial ischemia were examined in eight dogs. Regional ischemia was produced by selective microembolization of the left circumflex coronary artery. Mitral regurgitation and regional left ventricular wall motion abnormalities were evaluated with use of Doppler color flow mapping and two-dimensional echocardiography, respectively. Measurements were made at baseline (before embolization) and were repeated at 30 min and 3 weeks after embolization. Mitral regurgitation developed in all dogs 30 min after embolization and completely subsided 3 weeks later. There was no evidence of mitral valve prolapse, mitral anulus dilation or left ventricular segmental dyskinesia at any time during the study. Regional wall motion analysis showed only hypokinesia of the left ventricular segment overlying the papillary muscle at 30 min with subsequent normalization of the segment at 3 weeks. Mitral regurgitation was accompanied by an increase of the end-systolic distance between the mitral anulus plane and the point of coaptation of the mitral leaflets. This distance was 0.5 +/- 0.1 cm at baseline, increased to 0.9 +/- 0.1 cm 30 min after the embolization (p less than 0.001) and returned to near baseline (0.6 +/- 0.1 cm) 3 weeks after the embolization. These data indicate that mitral valve prolapse, mitral anulus dilation and regional left ventricular dyskinesia are not necessary conditions for the development of functional mitral regurgitation after acute myocardial ischemia. Instead, hypokinesia of the ventricular segment overlying the papillary muscle and leading to retraction of the mitral leaflets toward the apex appears to be a sufficient condition for incomplete leaflet coaptation.
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PMID:Mechanism of functional mitral regurgitation during acute myocardial ischemia. 155 1


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