Cardiomyopathy left ventricular hypertrophy

Cardiovascular diseases hypertension, coronary heart disease, cardiomyopathy, left ventricular hypertrophy, and arrhythmia. 

Mazur W, Nagueh SF Lakkis NM, et al. Regression of left ventricular hypertrophy after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. Circulation 2001 103 1492-1496. 

Aortic valve disease and hypertrophic obstructive cardiomyopathy with significant left ventricular hypertrophy Hypertension... 

Severe recurrent, but usually reversible hjrpertrophic cardiomyopathy has been infrequently reported, both in adults and children (SEDA-19, 352) (SEDA-20, 346). Based on experimental data and one additional case report, the interaction of tacrolimus with calcium channel blockers in the cardiac muscle has been suggested as a possible mechanism (SEDA-21, 390). However, the role of tacrolimus in the development of cardiomyopathy is still hjrpothetical. Echocardiographic abnormalities were relatively common before and after liver transplantation in 12 adult patients, and there was no clear evidence that oral tacrolimus specifically alters cardiac function (13). Other investigators did not show differences in heart weight, ventricular thickness, or valve circumferences between 67 Uver transplant recipients treated with tacrolimus and 72 non-transplanted patients who died from end-stage liver disease (14). In addition, more than 80% of patients in both groups had left ventricular hypertrophy. 

HOCM, Hypertrophic obstructive cardiomyopathy LVH, left ventricular hypertrophy 5 FU, 5 fluorouracil PE, pulmonary embolus PCI, percutaneous coronary mteivention TBSA, total surface body area ... 

Several disorders can impair ventricular function and play a role in the development of DHF. DHF is seen often in patients with hypertension, coronary artery disease (CAD), valvular heart disease, and hypertrophic cardiomyopathies. Hypertension is the most common underlying cardiovascular disorder in patients with DHF. There are several proposed mechanisms by which hypertension may impair diastolic function. Hypertension can alter diastolic function through its effects on (1) wall tension, (2) myocardial hypertrophy and fibrosis, and (3) small vessel structure and function, and (4) by predisposing to epicardial CAD. An association between impaired LV filling and subnormal high-energy phosphate metabolism has been shown in hypertensive patients, even in the absence of left ventricular hypertrophy (LVH). ... 

Spirito P, BelloneP, Harris KM, et al. Magnitudeof left ventricular hypertrophy and risk of sudden death in hypertrophic cardiomyopathy. N Engl JMed 2000 342 1778-1785. 

Numerous neuroendocrine biomarkers correlate with severity of cardiac dysfunction. Heart failure is associated with increase in peripheral vascular resistance due to increases in sympathetic tone, norepinephrine, renin, angiotensin II, arginine vasopressin, and endothelin-1. The increased venous pressure causes atrial distension that stimulates production and release of atrial and brain natriuretic peptides (ANP, BNP) from the atria and ventricles, respectively. ANP inhibits the renin-angiotensin-aldosterone system. In humans and mammals, BNP has been found to be an early biomarker of left ventricular hypertrophy developing with doxorubicin cardiotoxicity, congestive heart failure, or occult dilated cardiomyopathy (Erkus et al. 2006 Walker 2006 Oyama, Sisson, and Solter 2007). 

Ogino, K., Ogura, K., Kinugawa, T., Osaki, S., Kato, M., Furuse, Y, Kinugasa, Y, Tomikura, Y., Igawa, O., Hisatome, L, Shigemasa, C. (2004). Neurohumoral profiles in patients with hypertrophic cardiomyopathy differences to hypertensive left ventricular hypertrophy. Circ. J. 68 444—450. 

Cardiomyopathy [SED-15, 824 SEDA-32, 95], successfully treated with high-dose olanzapine, has been reported in a 17-year-old adolescent after the dose of clozapine was increased by 25 mg/day for 4 days to 375 mg/day after an initial dose of 275 mg/day [72 ]. His electrocardiogram showed a slightly prolonged QT<. interval, creatine kinase activity was raised at 462 U/1 (reference range 45-245 U/1), and there was reduced left ventricular function with left ventricular hypertrophy. The shortening fraction was 25% (reference range 30-42%). 

Some causes include left ventricular hypertrophy from prolonged hypertension, aortic stenosis, hypertrophic cardiomyopathy, and possibly myocardial fibrosis (in women)... 

Approximately 25% of all patients with hypertrophic cardiomyopathy (HCM) have latent left ventricular outflow obstruction with an intraventricular gradient (I). Pathophysiologic features are asymmetric hypertrophy of the septum and a systolic anterior movement of the anterior leaflet. Medical treatment includes betablockers, and calcium antagonists of the verapamil type. Approximately 5— 10% of the patients with outflow obstruction are refractory to such negative inotropic therapy (2). Positive inotropic drugs such as digitalis or sympathomimetics are strictly contraindicated. In the presence of atrial fibrillation, anticoagulation therapy should be started. Since endocarditis is more common in patients with HCM because of turbulence in the left ventricle, prophylactic antibiotics should be administered for periods of potential bacteraemia. 

By 5 hours of age, this infant was receiving glucose at a rate of 13 5 mg/kg/min. The blood glucose concentration continued to be less than 1.1 mmol/L, and the infant was given 15 mg of hydrocortisone every 6 hours. Echocardiography showed decreased left ventricular contractility and hypertrophy of the ventricular septum but no other structural abnormalities. These findings were consistent with the cardiomyopathy often seen in infants of diabetic mothers. 

Chronic use of metamfetamine has been associated with chronic coronary artery disease [12 , 13 ] as well as cardiomyopathy [14 ]. Recovery of left ventricular dysfunction in patients with metamfetamine-induced cardiomyopathy has been described [15 ]. However, since metamfetamine can cause myocyte hypertrophy [16, 17 ] and fibrosis [18 ], both relatively irreversible processes, it is likely that many patients will not recover left ventricular function, even with appropriate medical therapy or metamfetamine abstinence. 

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