UMLS:C0022116 - FACTA Search

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

Satisfactory NMR images of the heart can now be obtained using ECG gated inversion recovery and spin-echo sequences. The images obtained provide good anatomical information in the transverse, coronae, and sagittal planes, particularly of the myocardium and some intracardiac structures, such as cardiac valves and papillary muscle. The pericardium can be visualized, and so can the large vessels arising from the heart. Myocardial disease, in particular ischemia and infarction, is discussed in some detail, and mention is made of the cardiac aneurysms and various types of cardiomyopathy. Congenital heart disease and pericardial pathology are also briefly discussed.
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PMID:Nuclear magnetic resonance imaging of the heart. 308 96

We present our experience in the treatment of life-threatening ventricular tachycardia using electrophysiologically guided surgery (97 patients), automatic implantable cardioverter defibrillator (AICD) (42 patients), and orthotopic heart transplantation (15 patients). Eighty-three percent of these patients had ischemic and 17%, nonischemic heart disease. Our results of electrophysiologically directed surgery show an early mortality of 10% and a recurrence of 5% in the ischemic group. In the nonischemic group, the recurrence was 45%. The AICD was implanted in 31 patients with ischemic heart disease, in 5 with ventricular dysplasia, and in 6 with dilative cardiomyopathy, the ejection fractions ranging from 12% to 65%, with a mean of 30%. Early and late mortalities were 5% and 19%, respectively. The AICD was effective in all patients. Survival rate at 1 year was 83% +/- 6.4%. Thirteen of 15 patients have survived heart transplantation for 3-20 months (mean: 11 months). Ejection fractions prior to transplantation ranged from less than 10% to 34% (mean: 16%). We conclude that electrophysiologically guided surgery is highly effective in most cases of ischemia-related ventricular tachycardia. The AICD is considered a palliative alternative in patients with either poor ventricular function, no electrophysiological substrate, or multimorphological tachycardia. Heart transplantation has to be considered especially in young patients in whom progression of the underlying disease can be anticipated. Bridging by AICD is possible when transplantation is not immediately available or recommendable.
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PMID:Surgical alternatives in the treatment of life-threatening ventricular arrhythmias. 327 24

Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease of unknown cause that is characterized by a hypertrophied, nondilated, hypercontractile left ventricle. Its etiology and pathogenesis remain undefined but the three principal factors implicated are a genetic predisposition, a hypersensitivity to catecholamines, and an abnormal calcium metabolism. The hypertrophy typically involves the intraventricular septum to varying degrees, but may also involve the apex or free wall and even be concentric. The disease occurs in either an obstructive or a nonobstructive form depending on whether an intraventricular pressure gradient can be demonstrated at rest or on provocation. The gradient and obstruction to outflow is usually seen in patients with asymmetric septal hypertrophy (ASH) and anterior motion of the mitral valve during systole (SAM). Abnormal left ventricular diastolic function characterized by inadequate filling and impaired relaxation has been shown to be very important in both the obstructive and nonobstructive forms of the disease. In addition, inadequate coronary vasodilator reserve as a result of small vessel disease, microvascular spasm, and/or low capillary density per unit myocardial mass has been implicated as an important cause of ischemia in patients without coronary artery disease. HCM is a disease of young adulthood with relatively slow progression; young patients are often asymptomatic, whereas older patients are more limited by dyspnea, angina, dizziness, or syncope. Supraventricular tachyarrhythmias occur in 30% of patients, and high-grade ventricular arrhythmias occur in over 75%. The annual mortality is 3-5%. The common mode of demise is sudden cardiac death. Therefore, the primary objectives of treatment are the amelioration of symptoms, the control of arrhythmias, and the prevention of sudden death. Beta-adrenoreceptor blocking agents decrease myocardial contractility and oxygen demands and increase ventricular volume; therefore, they are most useful in patients with the obstructive form of HCM. Calcium channel antagonists enhance left ventricular relaxation, relieve microvascular spasm, and improve coronary filling and therefore are the agents of choice in patients with diastolic dysfunction. The ability of the calcium channel antagonists to decrease contractility makes them valuable in patients with obstructive HCM. Arterial vasodilators, diuretics, nitrates, and inotropic agents should be avoided because they can increase the intraventricular gradient. Myomyectomy is reserved for those patients with the obstructive form of HCM whose symptoms are refractory to medical therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypertrophic cardiomyopathy: current views on etiology, pathophysiology, and management. 331 Jun 37

To assess both ventricular function and myocardial perfusion, five normal volunteers, 19 patients with coronary artery disease, and two patients with cardiomyopathy and normal coronary arteries were injected with 20 mCi of Tc-99m isonitrile (either methoxyisobutyl isonitrile or carbomethoxyisopropyl isonitrile) at peak bicycle exercise and again at rest. A standard Tl-201 stress test was performed in all patients at the same level of exercise within one month of the isonitrile study. In all normal subjects, myocardial perfusion was normal at stress levels and the left ventricular ejection fraction increased 5% or more with exercise. In the 19 patients with coronary artery disease, the ejection fraction response to exercise was abnormal in 14 patients. Perfusion images with the Tc-99m isonitriles correlated well with Tl-201 images during exercise and at rest, with 89% concordance in areas of ischemia or infarction and 93% in normal segments. A simultaneous study of myocardial perfusion and ventricular function can be performed using a single Tc-99m labeled myocardial agent. Tc-99m isonitriles, particularly Tc-99m MIBI, result in sufficiently high photon flux that ventricular performance can be studied at peak exercise and again during rest using the first pass method.
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PMID:Simultaneous measurement of ventricular function and myocardial perfusion using the technetium-99m isonitriles. 334 20

Many patients with hypertrophic cardiomyopathy (HCM) have signs and symptoms or metabolic and hemodynamic evidence of myocardial ischemia and dysfunction in the absence of extramural coronary atherosclerosis. To investigate the possibility that a form of "small vessel disease" could account for these findings, a histologic analysis of left ventricular myocardium obtained at necropsy was carried out in 48 patients with hypertophic cardiomyopathy and in 68 controls with either normal hearts or acquired heart disease. In HCM, abnormal intramural coronary arteries (IMCA) were characterized by thickening of the vessel wall and an apparent decrease in luminal size (external arterial diameter less than 1500 micron; average 300 micron). The wall thickening was due to proliferation of medial and/or intimal components, particularly smooth muscle cells and collagen. Of the 48 patients with HCM,40 (83%) had abnormal IMCAs located in the ventricular septum (33 patients), anterior left ventricular free wall (20 patients) or posterior free wall (nine patients); an average of 3.0 +/- 0.7 IMCA were identified per tissue section. Altered IMCAs were also significantly more common in tissue sections having considerable myocardial fibrosis (31 out of 42, 74%) than in those with no or mild fibrosis (31 or 102, 30%; p less than 0.001). Abnormal IMCA wera also identified in 3 out of 8 infants who died of HCM before 1 year of age. In contrast, only rare altered IMCA were identified in six (9%) of the 69 control patients, and those arteries showed only mild thickening of the wall and minimal luminal narrowing (abnormal IMCA per section: 0.1 +/- 0.05: p less than 0.001). Moreover, of those patients who did show abnormal IMCA, such vessels were about twenty times more frequent in patients with HCM (0.9 +/- 0.2/cm2 myocardium) than in controls (0.04 +/- 0.02/cm2 myocardium). Hence, abnormal IMCA with markedly thickened walls and narrowed lumens are present in increased numbers in most patients with HCM at necropsy, and may represent a congenital component of the underlying cardiomyopathic process. Although the clinical significance of "small vessel coronary artery disease" in HCM is unclear, the occurrence of structurally altered IMCA within or adjacent to areas of substantial myocardial fibrosis suggests a causal role for these arteries in producing ischemia.
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PMID:Morphologic evidence for "small vessel disease" in patients with hypertrophic cardiomyopathy. 343 79

Between April 1983 and November 1985, 14 patients have undergone a heart transplant, or 10 men and 4 women, aged from 17 to 55 years. The surgical indication was a cardiomyopathy in terminal evolutive phase, of which the etiology was ischemia in 8 cases, congestion in 5 cases and rheumatism in one case. There was one operative death (7.1%) from acute rejection and a late death secondary to chronic rejection. The actuarial rate of survival at one and 2 years was 81.9%. Post-operative complications, most frequent at an early stage, were arterial hypertension (9 cases), rejection (8 cases) and renal insufficiency (6 cases). During an average post-operative evolution of 13 months, 17 rejection episodes occurred in 10 patients (71.4%) and 5 patients (35.7%) presented with 7 infectious episodes, one of them severe. Cyclosporin's toxicity appeared in the immediate post-operative period by an always reversible increase of the bilirubin and creatinin levels. On a long term, all patients present with arterial hypertension, accompanied by a moderate renal insufficiency (creatinin between 2.2 and 2.4 mg%). Among the survivors, 9 patients (75%) remain completely asymptomatic and have resumed normal physical activities. Cardiac transplantation has therefore become a valid therapeutic alternative, able to greatly improve survival and the functional condition of patients with terminal cardiomyopathy.
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PMID:[The surgical alternative in the treatment of terminal cardiomyopathies: cardiac transplantation]. 353 17

To determine the prevalence and significance of the systolic compression of the anterior descending coronary artery in hypertrophic cardiomyopathy, we studied 54 consecutive patients out of a catheterization laboratory population of 1619. This angiographic finding was found to be more prevalent (P less than 0.001) and severe in myopathic than in secondary hypertrophy. Complete systolic occlusion occurred in 5 of the 6 patients with nonobstructive cardiomyopathy showing the systolic narrowing. Severe septal squeezing was also present in these cases and the diastolic time lag to refill the distal branches reached 20-33% of the diastolic period. This subset of patients showed the least dynamic anterior wall contraction (P less than 0.001) and the highest incidence of thallium-201 perfusion defects (P less than 0.05) and of recurrent cardiac arrest (P less than 0.05). We conclude that severe systolic compression of the descending coronary artery in hypertrophic cardiomyopathy may be an angiographic marker of the myopathic hypertrophy extending to the anterior wall and might contribute to ischemia when the time to restore the distal perfusion is greatly delayed.
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PMID:Systolic compression of coronary artery in hypertrophic cardiomyopathy. 375 68

Diabetes mellitus is associated with a specific cardiomyopathy. This is evident from the clinical-pathological work and the epidemiologic data from the Framingham study. Noninvasive studies of diabetics have shown alterations in systolic and diastolic function that may ultimately lead to clinical heart failure. The relationship of these cardiac changes to the type of diabetes, its duration, and its severity is not settled. However, a correlation between changes in heart function and other complications of diabetes has been demonstrated. Insufficient prospective data is available from noninvasive studies to establish the frequency of progression from subclinical cardiac dysfunction to overt congestive failure. The pathogenesis of this disorder is still uncertain. Pathological studies have shown changes in the intramural arteries, arterioles, and capillaries but their functional significance is uncertain. Experimental studies have shown interstitial changes leading to an apparently less compliant left ventricle in the diabetic dog and monkey. In the diabetic rat reversible changes were found in myocardial function, related to changes in contractile proteins and intracellular calcium metabolism. In both species, the response to anoxia or ischemia was altered in the presence of diabetes. However, irreversible depression of the contractile element was not found in most animal studies of isolated diabetes. In contrast, the combination of hypertension and diabetes leads to substantial cardiac damage and circulatory congestion, both in clinical and experimental investigations. Clearly much more work must be carried out to understand the pathogenesis, treatment, and ultimately the prevention of diabetic cardiomyopathy.
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PMID:Diabetic cardiomyopathy. 388 Sep 19

This study was designed to determine whether human hearts release adenosine, a possible regulator of coronary flow, during temporary myocardial ischemia and, if so, to examine the mechanisms involved. Release of adenosine from canine hearts had been reported during reactive hyperemia following brief coronary occlusion, and we initially confirmed this observation in six dogs hearts. Angina was then produced in 15 patients with anginal syndrome and severe coronary atherosclerosis by rapid atrial pacing during diagnostic studies. In 13 of these patients, adenosine appeared in coronary sinus blood, at a mean level of 40 nmol/100 ml blood (SE = +/-9). In 11 of these 13, adenosine was not detectable in control or recovery samples; when measured, there was concomitant production of lactate and minimal leakage of K(+), but no significant release of creatine phosphokinase, lactic acid dehydrogenase, creatine, or Na(+). THERE WAS NO DETECTABLE RELEASE OF ADENOSINE BY HEARTS DURING PACING OR EXERCISE IN THREE CONTROL GROUPS OF PATIENTS: nine with anginal syndrome and severe coronary atherosclerosis who did not develop angina or produce lactate during rapid pacing, five with normal coronaries and no myocardial disease, and three with normal coronaries but with left ventricular failure. The results indicate that human hearts release significant amounts of adenosine during severe regional myocardial ischemia and anaerobic metabolism. Adenosine release might provide a useful supplementary index of the early effects of ischemia on myocardial metabolism, and might influence regional coronary flow during or after angina pectoris.
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PMID:Release of adenosine from human hearts during angina induced by rapid atrial pacing. 482 35

Ventricular ectopy occurs commonly. Its significance is related to the degree of complexity and the associated cardiac substrate. Coronary artery disease is the most frequent underlying cause, followed by cardiomyopathy and valvular disease. Symptomatic ventricular arrhythmias require treatment, whereas benign simple ventricular ectopy does not; however, the treatment of asymptomatic high-grade ventricular ectopy remains controversial. Therapy first must be directed toward the cardiac disease. Evaluation of the patient includes Holter monitoring, echocardiography, radionuclide studies, exercise testing, cardiac catheterization, and electrophysiologic testing. Programmed stimulation is useful in the diagnosis and prognosis of ventricular tachycardia, as well as in the evaluation of drug regimen efficacy. After treatment of ischemia and/or failure, specific antiarrhythmic agents, conventional and investigational, alone or in combination, are systematically selected. Should medical therapy alone be insufficient, consideration is given to surgical procedures such as subendocardial resection or ventriculotomy, often in combination with bypass grafting, aneurysmectomy, or valvular replacement. Electronic devices, including pacemakers or automatic internal defibrillators, may also be useful in certain selected cases. Suggested guidelines are proposed for a standardized approach, although therapy for each patient must still be individualized.
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PMID:Ventricular ectopy: etiology, evaluation, and therapy. 612 23

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