HIV-Associated Cardiomyopathy

Human immunodeficiency virus (HIV) disease is recognized as an important cause of dilated cardiomyopathy. Myocarditis and myocardial infection with HIV-1 are the best-studied causes of cardiomyopathy in HIV disease. HIV-1 virions appear to infect myocardial cells in a patchy distribution with no direct association between the presence of the virus and myocyte dysfunction. Myocardial dendritic cells seem to play a significant pathogenetic role by activating multifunctional cytokines (i. e., tumor necrosis factor-alpha) and the inducible form of nitric oxide synthase that contribute to progressive and late myocardial tissue damage. Coinfection with other viruses (usually, coxsackievirus B3 and cytomegalovirus) may also play an important etiopathogenetic role.The introduction of highly active antiretroviral therapy (HAART) has significantly reduced the incidence of myocarditis in HIV-infected patients living in developed countries. By contrast, in developing countries, where the availability of HAART is scanty and greater is the pathogenetic role of nutritional factors, the incidence of HIV-associated myocarditis and cardiomyopathy is increasing with a high mortality rate for congestive heart failure.A clinical diagnosis of myocarditis or congestive heart failure may be difficult in an HIV-infected patient due to masking of symptoms by concomitant bronchopulmonary disease and/or wasting syndromes, especially in a more advanced stage of HIV disease. Immunomodulatory therapy (intravenous immunoglobulins) may be helpful in adults and children with HIV-associated myocarditis and declining left ventricular function. Data on the role of HAART in the treatment of HIVassociated myocarditis and cardiomyopathy are lacking.     

Hypertrophic Cardiomyopathy

Opinion statement When an individual is diagnosed with hypertrophic cardiomyopathy (HCM), all relatives potentially affected by Mendelian autosomal-dominant inheritance should be evaluated with an electrocardiogram (ECG) and echocardiogram. Genetic testing should be considered in high-risk mutations where there are diagnostic uncertainties. Symptom relief depends on β-blockers as first-line therapy. If the disease is nonobstructive, then calcium channel blockers can be added or used alone. If there is a significant left ventricular outflow tract (LVOT) gradient then disopyramide can be used, ideally in combination with a β-blocker. Verapamil should be used with care due to potential exacerbation of the LVOT gradient. Nonmedical therapy for obstructive disease consists of surgical myectomy, alcohol septal ablation, or dual-chamber pacing. Surgery is the gold standard, although in experienced hands and directed appropriately, septal ablation achieves good results. Pacing is generally less effective. The development of atrial fibrillation (AF) or left atrial enlargement carries a significant risk of thromboembolism. All patients should be closely observed for AF and thromboembolic risk, and the threshold for initiation of anticoagulation should be low in patients with sustained palpitations, atrial enlargement, and nonsustained supraventricular arrhythmia on Holter. All patients with HCM should be assessed for their risk of sudden death regardless of severity of symptoms or morphology. The factors predictive of risk are 1) previous cardiac arrest; 2) unexplained syncope; 3) family history of premature sudden death; 4) abnormal blood pressure response to exercise; 5) nonsustained ventricular tachycardia; and 6) severe left ventricular hypertrophy ≥ 30 mm.     

心动过速性心肌病

心动过速性心肌病（TIC）是由持续或频发的室上性心动过速或室性心动过速所致的心肌疾病，患者没有器质性心脏病基础，发病与快速心室率有关，控制心室率后左室大小和功能可以全部或部分恢复正常。     

Stress-Induced Cardiomyopathy

No abstract available.     

Takotsubo Cardiomyopathy

Background  Takotsubo cardiomyopathy is a novel, yet well-described, reversible cardiomyopathy triggered by profound psychological or physical stress with a female predominance. Objective  This review is designed to increase general clinician awareness about the diagnosis, incidence, pathogenesis, and therapies of this entity. Data Sources  A complete search of multiple electronic databases (Pubmed, EMBASE, Science Citation Index) was carried out to identify all full-text, English-language articles published from 1980 to the present date and relevant to this review. Review Methods  The following search terms were used: takotsubo cardiomyopathy, stress-induced cardiomyopathy, and left ventricular apical ballooning syndrome. Citation lists from identified articles were subsequently reviewed and pertinent articles were further identified. Results  Takotsubo cardiomyopathy is typically characterized by the following: 1) acute onset of ischemic-like chest pain or dyspnea, 2) transient apical and mid-ventricular regional wall-motion abnormality, 3) minor elevation of cardiac biomarkers, 4) dynamic electrocardiographic changes, and 5) the absence of epicardial coronary artery disease. The pathogenesis of the syndrome is unknown but has mostly been associated with acute emotional or physiologic stressors. Dote, Sato, Tateishi, Uchida, Ishihara (J Cardiol. 21(2):203–214, 1991); Desmet, Adriaenssens, Dens (Heart. 89(9):1027–1031, Sep., 2003); Bybee, Kara, Prasad, et al. (Ann Intern Med. 141(11):858–865, Dec 7, 2004); Sharkey, Lesser, Zenovich, et al. (Circulation. 111(4):472–479, Feb 1, 2005) The short and long-term prognosis of these patients is overwhelmingly favorable and often only requires supportive therapy. Conclusion  Whether an emotional or physical event precedes one’s symptoms, it is apparent that takotsubo cardiomyopathy case presentations mimic ST-segment elevation myocardial infarction, and thus is an important entity to be recognized by the medical community.