الفهرس 
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Abstract
HCM is characterized by a thickened but nondilated left ventricle in the absence of another cardiac or systemic condition capable of producing the magnitude of hypertrophy evident (e.g., aortic valve stenosis, systemic hypertension, and some expressions of athlete’s heart). The histologic features of HCM are disarray of cell to cell arrangement, disorganization of cellular architecture, and fibrosis (Maro et al, 1981).
HCM is transmitted as a mendelian trait with an autosomal dominant pattern of inheritance. Molecular studies, conducted intensively over more than a decade, have provided access to definitive laboratory-based diagnosis by detecting pathological disease-causing mutations (even without obvious clinical evidence of the disease), affording important insights into the broad clinical expression of HCM and genetic counseling, as well as promoting recognition of greater numbers of patients (Seidman, 2002).
Transplantation is the only option for patients with severely symptomatic, nonobstructive HCM. However; persons with obstruction who continue to have symptoms despite optimal medical treatment are candidates for septal myotomy-myectomy with or without mitral valve replacement, alcohol septal ablation, and dual-chamber pacing (Biagini et al, 2008).
Surgical myectomy is regarded as first-line treatment for symptoms caused by resting or provocable LV obstruction. Data accumulated over 40 years show that myectomy reduces obstruction-related symptoms effectively and is associated with low mortality, and a reduced risk of sudden death compared with those who were treated pharmacologically. Intraoperative echocardiography is an important guide for determining the extension of myectomy. In patients with primary valve abnormalities or minimal septal hypertrophy in the target zone, mitral valve repair or replacement should be carried out (Schulte et al, 1999).
Dual-Chamber Pacing, initial reports of symptom relief and decrease LVOT (left ventricular out flow tract) obstruction with dual-chamber pacing have been questioned. Pacing may have deleterious effects on ventricular filling and cardiac output .The latest pacing guidelines indicate that pacing should only be considered in patients with drug refractory HCM with resting or provoked LVOT gradient and contraindications for septal ablation or myectomy. It is done through placing the pacemaker tip in the apex of right ventricle to achieve the greatest reduction in the gradient (Betocchi et al, 1996).
Lastly it is proved that neurohormonal antagonism potentially has pleiotropic benefits including suppression of: tissue/systemic neuroendocrine activation, electrolyte defects (K+and Mg2+), fibroblast activity with collagen deposition (eg, via BMP-7/TGF-β1) and mitigation of microvasculopathy, which may have pathophysiological and prognostic benefits in HCM using ACE-I/ARBs/spironolactone, diminished microvasculopathy, fibrosis, cardiac dysfunction, and adverse symptoms (O’Hanlon et al, 2010). Other pharmacological approaches to mitigating LVH include rapamycin (inhibiting the mammalian target of rapamycin-mTOR), which exhibits antihypertrophic properties in rodents. In practice, derivatives or substitutes of such agents will likely be required because of their immunosuppressive effects (Day et al, 2009).