Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Important sex differences in cardiovascular disease outcomes exist, including conditions of hypertrophic cardiomyopathy and cardiac ischemia. Studies of sex differences in the extent to which load-independent (primary) hypertrophy modulates the response to ischemia-reperfusion (I/R) damage have not been characterized. We have previously described a model of primary genetic cardiac hypertrophy, the hypertrophic heart rat (HHR). In this study the sex differences in HHR cardiac function and responses to I/R [compared to control normal heart rat (NHR)] were investigated ex vivo. The ventricular weight index was markedly increased in HHR female (7.82 +/- 0.49 vs. 4.80 +/- 0.10 mg/g; P < 0.05) and male (5.76 +/- 0.22 vs. 4.62 +/- 0.07 mg/g; P < 0.05) hearts. Female hearts of both strains exhibited a reduced basal contractility compared with strain-matched males [maximum first derivative of pressure (dP/dt(max)): NHR, 4,036 +/- 171 vs. 4,258 +/- 152 mmHg/s; and HHR, 3,974 +/- 160 vs. 4,540 +/- 259 mmHg/s; P < 0.05]. HHR hearts were more susceptible to I/R (I = 25 min, and R = 30 min) injury than NHR hearts (decreased functional recovery, and increased lactate dehydrogenase efflux). Female NHR hearts exhibited a significantly greater recovery (dP/dt(max)) post-I/R relative to male NHR (95.0 +/- 12.2% vs. 60.5 +/- 9.4%), a resistance to postischemic dysfunction not evident in female HHR (29.0 +/- 5.6% vs. 25.9 +/- 6.3%). Ventricular fibrillation was suppressed, and expression levels of Akt and ERK1/2 were selectively elevated in female NHR hearts. Thus the occurrence of load-independent primary cardiac hypertrophy undermines the intrinsic resistance of female hearts to I/R insult, with the observed abrogation of endogenous cardioprotective signaling pathways consistent with a potential mechanistic role in this loss of protection.
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PMID:The intrinsic resistance of female hearts to an ischemic insult is abrogated in primary cardiac hypertrophy. 1824 62

Focal tissue abnormalities consistent with regional ischemia have been reported in patients with hypertrophic cardiomyopathy (HCM). Coronary microvascular dysfunction has been also reported to be present in patients with HCM despite normal epicardial coronary arteries. Moreover, it has been demonstrated that in the case of HCM and idiopathic left ventricular hypertrophy, hypoplastic coronary arteries as diminutive vessels are present and that obstructive hypertrophic cardiomyopathy is associated with enhanced thrombin generation and platelet activation. Previously, it has been described an acute myocardial infarction in a young athlete with non-obstructive hypertrophic cardiomyopathy and normal coronary arteries. We present a case of an acute myocardial infarction with diminutive right coronary artery and obstructive hypertrophic cardiomyopathy without significant coronary stenoses. To our knowledge, this is the first report of an acute myocardial infarction with diminutive right coronary artery and obstructive hypertrophic cardiomyopathy without significant coronary stenoses.
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PMID:Acute myocardial infarction with diminutive right coronary artery and obstructive hypertrophic cardiomyopathy without significant coronary stenoses. 1863 52

Cocaine is the second most commonly abused illicit drug in the US and the most common one involved in emergency department visits, the majority of which are related to the cardiovascular system. Cardiovascular complications related with cocaine abuse include myocardial ischemia and infarction, myocarditis, hypertrophic cardiomyopathy, dilated cardiomyopathy, aortic dissection, thrombosis, stroke and cerebral hemorrhage, and different forms of visceral ischemia, among others. In an era where cocaine use has reached epidemic proportions, it is necessary for the radiologist to understand the pathophysiology, clinical presentation, and imaging characteristics of its cardiovascular complications.
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PMID:Cardiovascular complications of cocaine: imaging findings. 1877 29

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

After hypertrophic cardiomyopathy, coronary artery anomalies of origin from the wrong sinus of Valsalva are the second most common cause of sudden death on the athletic field in the USA. Although the right coronary artery arising from the left coronary sinus (ARCA) is four times as common as the left coronary artery arising from the anterior sinus (ALCA), it is the latter that is by far the more common cause of sudden death with or shortly after vigorous physical activity. Of the four types of ALCA, the interarterial type, where the left coronary artery passes anteriorly between the aorta and the right ventricular outflow tract, is the only type that places the patient at risk of sudden death. Another feature of this syndrome is the fact that sudden death occurs associated with or shortly after vigorous exercise and is very unusual after the patient is > 35 years of age. The mechanism by which there is sudden occlusion of the interarterial coronary artery is at present unknown, although there are a number of hypotheses involving the oblique passage of the vessel as it leaves the aorta. Sudden death is probably rare considering the number of people who have these anomalies. Symptoms premonitory to a fatal event such as exertional syncope, chest pain, or palpitations are probably common in patients at risk, and surgical correction is indicated in symptomatic patients at any age. In older asymptomatic patients, surgery is not recommended, since the incidence of sudden death in this age group is extremely small. In asymptomatic young patients, a stress test, preferably with radioisotope myocardial perfusion imaging or stress echocardiogram, should be done and surgical correction performed in those with ischemia provoked in the appropriate myocardial region. Since there is evidence that in patients who have survived a potentially fatal event, it is rare to be able to provoke ischemia with equal or greater exercise than had precipitated the malignant arrhythmia, the decision to surgically correct an asymptomatic young patient, serendipitously found to have ALCA, who has a negative exercise test, is debatable. Any decision for surgery in such patients should be made only after a full discussion of the risks pro and con surgery with the patient and the patient's family.
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PMID:Congenital anomalies of coronary arteries: role in the pathogenesis of sudden cardiac death. 1957 57

Since its original description 50 years ago, myocardial ischemia has been a recognized but underappreciated aspect of the pathophysiology of hypertrophic cardiomyopathy (HCM). Nevertheless, the assessment of myocardial ischemia is still not part of routine clinical diagnostic or management strategies. Morphologic abnormalities of the intramural coronary arterioles represent the primary morphologic substrate for microvascular dysfunction and its functional consequence-that is, blunted myocardial blood flow (MBF) during stress. Recently, a number of studies using contemporary cardiovascular imaging modalities such as positron emission tomography (PET) and cardiovascular magnetic resonance (CMR) have led to an enhanced understanding of the role that myocardial ischemia and its sequelae fibrosis play on clinical outcome. In this regard, studies with PET have shown that HCM patients have impaired MBF after dipyridamole infusion and that this blunted MBF is a powerful independent predictor of cardiovascular mortality and adverse LV remodeling associated with LV systolic dysfunction. Stress CMR with late gadolinium enhancement (LGE) has also shown that MBF is reduced in relation to magnitude of wall thickness and in those LV segments occupied by LGE (i.e., fibrosis). These CMR observations show an association between ischemia, myocardial fibrosis, and LV remodeling, providing support that abnormal MBF caused by microvascular dysfunction is responsible for myocardial ischemia-mediated myocyte death, and ultimately replacement fibrosis. Efforts should now focus on detecting myocardial ischemia before adverse LV remodeling begins, so that interventional treatment strategies can be initiated earlier in the clinical course to mitigate ischemia and beneficially alter the natural history of HCM.
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PMID:The case for myocardial ischemia in hypertrophic cardiomyopathy. 1969 69

Hypertrophic cardiomyopathy (HCM) is the most common cause of sudden cardiac death in young people. The implantable cardioverter-defibrillator (ICD), has recently proved to be a safe and effective therapeutic intervention in patients with HCM, both for the primary and secondary prevention of sudden death. Based on recent substantial experience, the ICD intervenes appropriately to terminate ventricular tachycardia/fibrillation (VT/VF), at a rate of 5.5%/year. ICD discharge rate is 4%/year in those patients implanted prophylactically due to one or more major risk markers, but often with considerable delays of up to 10 years before the device is required to intervene appropriately to terminate potentially letal ventricular tachyarrhythmias. Primary prevention of VT/VF occurs with similar frequency in high-risk patients having either 1, 2 or > or =3 noninvasive risk markers, and about one-third of patients with appropriate device interventions had been implanted for only one risk factor. The ICD has proved reliable in HCM despite the extreme and complex phenotypes often present with massive degrees of left ventricular hypertrophy, microvascular ischemia, diastolic dysfunction, or dynamic left ventricular outflow tract obstruction. Failure to convert life-threatening ventricular tachyarrhythmias to normal rhythm is extraordinarily rare. In conclusion, in high-risk HCM patients, ICDs perform in a highly effective fashion, frequently preventing sudden death by aborting primary life-threatening ventricular tachyarrhythmias. A single marker of high risk can be sufficient evidence to justify the recommendation for a prophylactic ICD in selected patients with HCM.
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PMID:[Prevention of sudden death in hypertrophic cardiomyopathy (HCM ): implanted defibrillators in HCM]. 1979 62

Hypertrophic cardiomyopathy (HCM) is characterized by extreme clinical heterogeneity, ranging from sudden cardiac death to long-term disease progression and heart failure-related complications. Myocardial ischemia, occurring at the microvascular level, is a major determinant of clinical expression and outcome. Accordingly, the severity of this microvascular dysfunction has been shown to represent an early and powerful predictor of unfavorable outcome in HCM. The assessment of microvascular function in vivo is technically challenging, although critical to a truly comprehensive evaluation and risk stratification of HCM patients. Available technologies include positron emission tomography and cardiac magnetic resonance (CMR). Studies of regional myocardial blood flow using positron emission tomography have demonstrated that the vasodilator response to dipyridamole is impaired in most HCM patients, not only in the hypertrophied ventricular septum but also in the less hypertrophied or non-thickened left ventricular free wall. CMR also allows measurement of myocardial flow, although the technique is currently time-consuming and largely limited to research situations. CMR provides further insight into the effects of ischemia in HCM patients, by visualizing the distribution and extent of fibrosis at the intramyocardial level. Late gadolinium enhancement (LGE) is a potential predictor of risk in HCM patients, and is believed to largely reflect replacement fibrosis resulting from recurrent microvascular ischemia. LGE is associated with increased prevalence of ventricular arrhythmias, and associated with microvascular dysfunction. The present review is to provide a concise overview for the available evidence of microvascular ischemia and its consequences in HCM.
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PMID:[Myocardial hypoperfusion due to microvascular dysfunction in hypertrophic cardiomyopathy: role of positron emission tomography]. 2019 74

Hypertrophic cardiomyopathy (HCM) is one of the most common inherited cardiomyopathy. The identification of patients with HCM is sometimes still a challenge. Moreover, the pathophysiology of the disease is complex because of left ventricular hyper-contractile state, diastolic dysfunction, ischemia and obstruction which can be coexistent in the same patient. In this review, we discuss the current and emerging echocardiographic methodology that can help physicians in the correct diagnostic and pathophysiological assessment of patients with HCM.
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PMID:Echocardiography in patients with hypertrophic cardiomyopathy: usefulness of old and new techniques in the diagnosis and pathophysiological assessment. 2023 38

The risk of sudden cardiac death (SCD) associated with vigorous athletic competition in individuals with hypertrophic cardiomyopathy (HCM) is well documented, and is the basis for recommended exclusion from competitive sports independent of other risk factors. Although SCD risk with recreational exercise is less well defined, published guidelines for participation in recreational sports, based on a consensus of expert opinion, offer a valuable framework for counseling patients. Exercise stress testing is an important diagnostic and prognostic tool in the evaluation of HCM patients, providing an objective measure of functional capacity, physiologic hemodynamic responses to stress, presence of ischemia, and provocable left ventricular outflow tract obstruction. The value of cardiopulmonary exercise testing in HCM is less well studied than in the heart failure population, but can be used to set a safe target for exercise intensity as part of an individualized exercise prescription. The long-term effects of exercise on HCM pathophysiology are largely theoretical at this stage. Potential harmful effects of fatiguing exercise include prolonged contractile dysfunction resulting from microvascular ischemia and energetic compromise. Conversely, several animal studies have shown that voluntary exercise prevents or reverses many pathologic features of HCM, including those related to apoptosis and energetics. Substantial evidence for health-promoting benefits of exercise in the general population, in addition to promising safety and efficacy data in patients with chronic heart failure, emphasizes the need to attain a reasonable balance between potential risks and benefits of aerobic fitness in individuals with HCM.
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PMID:Exercise in hypertrophic cardiomyopathy. 2055 99


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