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)

Familial hypercholesterolemia (FH) is an autosomal dominant disorder characterized by a high level of LDL-cholesterol and frequent coronary atherosclerosis. We studied a 64 year old woman with heterozygous (hetero) FH, who showed symptoms of chest pain and dyspnea with no other coronary risk factors than post-menopause and hypercholesterolemia. Although her coronary symptoms didn't reveal significant stenosis on coronary angiography, she had severe aortic valvular and supravalvular stenosis at the ascending aorta, which qualified her for aortic valve replacement. Moreover, a coronary flow study revealed functional ischemia with a reduction of the coronary flow reserve. We report a case of valvular and supravalvular aortic stenosis corrected by aortic valve replacement, a rare complication of hetero FH.
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PMID:Valvular and supravalvular aortic stenosis in heterozygous familial hypercholesterolemia, a case report. 1620 26

Presently, conventional wisdom is that an asymptomatic patient, even with severe aortic stenosis (AS), can be followed medically. The basis for this recommendation is that sudden death as the first "symptom" in an asymptomatic patient is rare. Unfortunately, symptoms are subjective and can be ignored or explained away by both patient and physician, and once symptoms are recognized, sudden death accounts for at least one third of the deaths from AS in unoperated patients. There is evidence that once AS becomes severe, ischemia and fibrosis occur rapidly, setting up the possibility of heart failure and sudden death even after successful valve replacement. Aortic valve replacement should be performed before extensive fibrosis occurs. Multiple studies have shown that in severe AS, symptoms will occur rapidly when there is heavy valve calcification, an aortic valve area <0.8 cm, an annual rate of progression of aortic valve velocity of >/=0.3 m/sec, or a positive exercise stress test. These findings are excellent evidence that asymptomatic patients with severe AS and any of the above findings should be considered for aortic valve replacement.
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PMID:Asymptomatic adult patients with aortic stenosis: should they ever have aortic valve replacement? 1633 Sep 16

Ongoing myocardial thickening after aortic valve closure (postsystolic thickening = epsilonPST) is an established marker for the presence of segmental ischemia. However, epsilonPST may also be present in late activated segments and can be induced by pharmacological interventions or left ventricular pressure overload. The aim of this study was to determine if it is possible to distinguish between ischemic and nonischemic epsilonPST. In an experimental pig-model (n = 11) regional radial deformation was measured in the inferolateral wall during either normal perfusion or regional ischemia using ultrasonic strain rate imaging. Ischemia was induced by active hypoperfusion of the circumflex coronary artery territory. Measurements were made at 1. baseline, and during 2. theodrenalin infusion, 3. dobutamine infusion 4. esmolol infusion and 5. during a preload increase induced by saline infusion. In all segments where thickening was ongoing after aortic valve closure, the amount of epsilonPST was calculated as the difference of maximal strain minus systolic strain. In addition, peak strain rate during the isovolumetric relaxation period was extracted. During normal coronary perfusion, 73% of all segments (n = 40) developed epsilonPST. This physiological epsilonPST averaged 5 +/- 2% and was most frequently induced during the esmolol infusion (n = 11). Peak isovolumetric strain rate averaged -2.1 +/- 0.5 s(-1) in segments with physiological epsilonPST. During coronary hypoperfusion, 96% of the "at risk" segments developed epsilonPST. EpsilonPST in the ischemic segments averaged 14 +/- 3%, and was highest during the dobutamine infusion (25 +/- 4%) and lowest during the esmolol infusion (5 +/- 1%). In contrast to normally perfused segments, peak isovolumetric strain rate was positive in the ischemic segments and averaged 2.0 +/- 0.5 s(-1) in these pathologic segments with postsystolic strain. Using a cut-off value of > or = 0 s(-1) for isovolumetric strain rate, pathologic epsilonPST was detected with a sensitivity of 100% and a specificity of 87%. These experimental findings were confirmed by a subsequent clinical study with 6 patients with acute myocardial infarction (ischemic group) and 6 patients with arterial hypertension or aortic stenosis (nonischemic group). Ischemic and nonischemic postsystolic thickening can be precisely differentiated by extracting the polarity of the peak isovolumetric strain curve.
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PMID:How to distinguish between ischemic and nonischemic postsystolic thickening: a strain rate imaging study. 1636 97

Transient ischemic dilatation (TID) of the left ventricle observed during single photon myocardial perfusion emission computed tomography (SPECT) is an important non-perfusion finding that may not only suggest underlying significant (usually multi-vessel) coronary artery disease (CAD) but also an independent prognostic factor of adverse outcomes regardless of abnormal or normal perfusion finding. We present a patient with no significant epicardial coronary disease who had significant TID and considerable decrease in the left ventricular ejection fraction with left ventricular dilatation after a rest-stress Tc-99 tetrofosmin SPECT study in the setting of severe aortic stenosis. With the advent of gated SPECT imaging the additive value of determining rest and post stress EF, as demonstrated in this case, aided in the recognition of TID and transient decrease in the left ventricular ejection fraction. These are not necessarily related to obstructive epicardial coronary disease, but are a result of severe aortic valve disease causing subendocardial ischemia in the setting of multilple other non-ischemic etiologies of TID such as left ventricular hypertrophy and diabetes mellitus.
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PMID:Transient ischemic dilatation of the left ventricle with severe post stress left ventricular dysfunction in the setting of severe aortic stenosis and normal coronary arteries. 1692 2

The burden of aortic stenosis is increasing steadily and, despite major advances in diagnosis and management, surgical valve replacement is still the only effective treatment. Most recently, experimental studies in animals and clinical studies in humans have shown that myocardial hypertrophy, microcirculatory dysfunction and cardiomyocyte apoptosis are among the central pathophysiologic mechanisms involved in the natural history of aortic stenosis, i.e. the passage from a compensated and hypertrophic heart to a dysfunctional heart prone to ischemia, arrhythmia and pump failure. This updated review emphasizes the promises of these new research avenues as well as their potential therapeutic applications.
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PMID:[Pathophysiologic role of myocardial hypertrophy, microcirculatory dysfunction and cardiomyocyte apoptosis in aortic stenosis]. 1697 83

Gastric cancer was detected in a 71-year-old man with severe aortic stenosis. According to ACC/AHA guidelines, aortic stenosis in the patient was so severe that noncardiac surgery was considered appropriate only after aortic valve replacement. However, due to uncontrollable hemorrhage from gastric cancer, total gastrectomy was urgently required. Surgery was performed under epidural and general anesthesia. Blood pressure and heart rate were stable during anesthetic induction, tracheal intubation and skin incision. Just after peritoneal incision, however, ST decreased significantly following hypertension and sinus tachycardia, which were controllable by deepening of the anesthetic level. This ST depression was dependent on heart rate but not blood pressure. Therefore, in order to control the heart rate and prevent myocardial ischemia, low dose landiolol was infused prophylactically. This agent regulated the heart rate below 85 beats per minute without inducing hypotension and prevented myocardial ischemia during the remaining anesthetic course including extubation and recovery from anesthesia. Although beta blocker is not generally recommended in patients with aortic stenosis, present case suggests that landiolol is effective and useful to prevent cardiac ischemia even in a patient with severe aortic stenosis.
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PMID:[Landiolol prevented myocardial ischemia in a patient with severe aortic stenosis undergoing total gastrectomy]. 1751

Hypertrophic cardiomyopathy (HCM) is classified as a primary cardiomyopathy. HCM is a clinically heterogeneous but relatively common autosomal dominant genetic heart disease that probably is the most frequently occurring cardiomyopathy. HCM is characterized morphologically and defined by a hypertrophied, nondilated left ventriculum (LV) in the absence of another systemic or cardiac disease that is capable of producing the magnitude of wall thickening evident (e.g., systemic hypertension, aortic valve stenosis). Most HCM patients have the propensity to develop dynamic obstruction to LV outflow under resting or physiologically provocable conditions, produced by systolic anterior motion of the mitral valve with ventricular septal contact. The phenotypic features of HCM may develop at any age from infancy to adulthood, and are characterized by a great heterogeneity in the extent, magnitude, and distribution of left ventricular hypertrophy. Hypertrophic obstructive cardiomyopathy (HOCM) often leads to heart failure, severe ischemia, severe symptoms and death. Determination of the exact site of the hypertrophy and of the obstruction of the left ventricular outflow tract, in asymmetric septal hypertrophy, establishes which is the best treatment strategy. In the treatment of HOCM, drug therapy with negatively inotropic drugs, percutaneous transluminal septal myocardial ablation by alcohol-induced septal branch occlusion, surgical myectomy and DDD pacemaker therapy are considered the therapeutical options. We present a case of an obstructive hypertrophic cardiomyopathy in an 84-year-old Italian woman with a left ventricular outflow tract (LVOT) peak gradient with the Valsalva maneuver of 188 mm Hg and with a history of first episode of syncope.
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PMID:Revelation of an obstructive hypertrophic cardiomyopathy in an elderly patient. 1918 3

Stress echocardiography is increasingly used but its major limitation is the subjective interpretation of wall motion changes requiring experience. Speckle tracking enables simultaneous evaluation of radial, longitudinal, and circumferential myocardial deformation. Recently, two-dimensional (2D) strain has been found to be as reliable as sonomicrometry for the assessment of left ventricular (LV) regional function. In the presence of inducible ischemia, longitudinal and circumferential abnormalities preceed the decrease in radial deformation. Optimal cutoffs have been obtained from 2D strain rate (SR) at peak dobutamine stress to predict coronary artery disease. However, 2D strain rate does not yet provide incremental accuracy to visual interpretation by experts. Speckle tracking strain could be useful to better identify contractile reverse and biphasic response of viable myocardium but there are not yet clinical studies published in this setting. Preliminary results suggest that 2D strain obtained during exercise could be useful in asymptomatic patients with severe aortic stenosis or organic mitral regurgitation (MR). In conclusion, the reliability and clinical importance of 2D strain during stress will be specified by further investigations.
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PMID:The value of 2D strain imaging during stress testing. 1929 Oct 14

Anginal chest pain is one of the most common complaints in the outpatient setting. While much of the focus has been on identifying obstructive atherosclerotic coronary artery disease (CAD) as the cause of anginal chest pain, it is clear that microvascular coronary dysfunction (MCD) can also cause anginal chest pain as a manifestation of ischemic heart disease, and carries an increased cardiovascular risk. Epicardial coronary vasospasm, aortic stenosis, left ventricular hypertrophy, congenital coronary anomalies, mitral valve prolapse, and abnormal cardiac nociception can also present as angina of cardiac origin. For nonacute coronary syndrome (ACS) stable chest pain, exercise treadmill testing (ETT) remains the primary tool for diagnosis of ischemia and cardiac risk stratification; however, in certain subsets of patients, such as women, ETT has a lower sensitivity and specificity for identifying obstructive CAD. When combined with an imaging modality, such as nuclear perfusion or echocardiography testing, the sensitivity and specificity of stress testing for detection of obstructive CAD improves significantly. Advancements in stress cardiac magnetic resonance imaging enables detection of perfusion abnormalities in a specific coronary artery territory, as well as subendocardial ischemia associated with MCD. Coronary computed tomography angiography enables visual assessment of obstructive CAD, albeit with a higher radiation dose. Invasive coronary angiography remains the gold standard for diagnosis and treatment of obstructive lesions that cause medically refractory stable angina. Furthermore, in patients with normal coronary angiograms, the addition of coronary reactivity testing can help diagnose endothelial-dependent and -independent microvascular dysfunction. Lifestyle modification and pharmacologic intervention remains the cornerstone of therapy to reduce morbidity and mortality in patients with stable angina. This review focuses on the pathophysiology, diagnosis, and treatment of stable, non-ACS anginal chest pain.
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PMID:Nonacute coronary syndrome anginal chest pain. 2038 Sep 51

Serum cardiac troponins I and T are reliable and highly specific markers of myocardial injury. Studies have shown that at least 20% of patients with severe aortic stenosis have detectable serum troponins. This case report describes a patient who presented as suspected acute coronary syndrome with markedly elevated troponin levels, who was later found to have normal coronaries and critical aortic stenosis. This case highlights the need for comprehensive and accurate physical examination in patients who present with angina. Critical aortic stenosis may cause such severe subendocardial ischemia as to cause marked elevation in cardiac markers and mimic an acute coronary syndrome. Careful physical examination will lead to an earlier use of non invasive techniques, such as echocardiography to confirm the correct diagnosis and the avoidance of inappropriate treatments such as intravenous nitroglycerin and glycoprotein IIb/IIIa inhibitors.
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PMID:A case of critical aortic stenosis masquerading as acute coronary syndrome. 2072 Dec 72


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