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Query: UMLS:C0205700 (ash)
 15,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Asymmetric septal hypertrophy is considered by many to be pathologic but its presence in a number of states associated with left ventricular overload indicates that it may develop as an adaptive feature in the overloaded heart. This hypothesis implies that initially in these states a greater systolic stress and thus energy metabolism occurs in the ventricular septum than in the left ventricular free wall. It was previously demonstrated that in the early stages of ischemia regional differences in energy metabolism could be determined by comparisons of tissue high energy phosphate depletion and lactate accumulation. In the present study these measurements were made in an animal model of left ventricular overload. In open chest dogs aortic insufficiency was produced, which served to provide both volume overload to the left ventricle and regional myocardial ischemia. In addition to regional metabolite levels, measurements of regional blood flow were determined using radioactive microspheres. Tissue samples were taken from the left ventricle and interventricular septum, freeze clamped, divided transmurally into thirds and analyzed for creatine phosphate, adenosine triphosphate and lactate. Animals with myocardial ischemia after aortic insufficiency were classified into two groups: those in which ischemia was limited to the inner left ventricle and left side of the septum and those with more extensive ischemia transmurally. In the latter group, creatine phosphate depletion and lactate accumulation were greater in the septum, but myocardial blood flow was also more depressed in the septum than in the left ventricle. In the former group, where ischemia was more restricted, metabolite changes were also more severe in the left septum than in the inner left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional blood flow and metabolite levels in the left ventricular free wall and septum during aortic insufficiency: implications for the development of asymmetric septal hypertrophy. 294 41

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

Pain thresholds in humans were determined for heat stimulations of the skin before and after a mild injury induced by a single conditioning stimulus (CS) of 50 degrees C and 100 sec duration. The same stimuli were delivered to the receptive fields of C fiber and A fiber mechanoheat-sensitive nociceptors (CMH and AMH nociceptors, respectively) and of low threshold warm and cold receptors in the anesthetized monkey and to the receptive fields of CMH nociceptors recorded percutaneously from the peroneal nerve of awake humans. Pain thresholds in normal skin were matched only by the response thresholds of CMH and not AMH nociceptors. Immediately following heat injury, some pain thresholds and CMH response thresholds were elevated, but by 5 to 10 min after the CS, pain and CMH thresholds were lowered to 2 to 6 degrees C below normal (hyperalgesia and nociceptor sensitization). No other type of cutaneous receptor studied exhibited changes in threshold similar to those observed for pain and for CMH nociceptors. The magnitude of hyperalgesia in humans and the magnitude of sensitization of CMH nociceptors in monkeys following heat injury were greater for hairy than for glabrous skin. The time course of the development of hyperalgesia was not altered by ischemia or conduction block in A fibers. The results support the conclusion that altered activity in CMH nociceptors is a major peripheral determinant of cutaneous hyperalgesia following a mild heat injury to the skin.
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PMID:Peripheral neural mechanisms of cutaneous hyperalgesia following mild injury by heat. 708 82

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

Hypoxic preconditioning reduces disease severity in a mouse model of multiple sclerosis (MS), in part by enhancing the barrier properties of spinal cord blood vessels. Because other studies have shown that similar levels of hypoxia transiently increase permeability of central nervous system (CNS) blood vessels, the goal of this study was to define the impact of chronic mild hypoxia (CMH, 8% O2) on the integrity of spinal cord blood vessels and the responses of neighboring glial cells. Using extravascular fibrinogen as a marker of vascular disruption, we found that CMH triggered transient vascular leak in spinal cord blood vessels, particularly in white matter, which was associated with clustering and activation of Mac-1-positive microglia around disrupted vessels. Microglial depletion with the colony stimulating factor-1 receptor (CSF-1R) inhibitor PLX5622, while having no effect under normoxic conditions, profoundly increased vascular leak in both white and gray matter during CMH, and this was associated with disruption of astrocyte-vascular coupling and enhanced loss of tight junction proteins. Microglial repair of leaky blood vessels was blocked by a peptide that inhibits the interaction between fibrinogen and its Mac-1 integrin receptor. These findings highlight an important role for microglia in maintaining vascular integrity in the hypoxic spinal cord and suggest that a fibrinogen-Mac-1 interaction underpins this response. As relative hypoxia is experienced in many situations including high altitude, lung disease, obstructive sleep apnea, and age-related CNS ischemia/hypoxia, our findings have important implications regarding the critical role of microglia in maintaining vascular integrity in the CNS.
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PMID:A critical role for microglia in maintaining vascular integrity in the hypoxic spinal cord. 3177 11