Carnitine levels in patients with chronic rheumatic heart disease.
ABSTRACT Carnitine, a small aminoacid derivative plays a major role in fatty acid oxidation. Myocardial carnitine deficiency may cause malfunction of the heart. Rheumatic valvular heart disease can be associated with myocardial dysfunction. We have investigated myocardial and plasma-free carnitine levels in patients with chronic rheumatic heart disease.
Eleven patients with chronic rheumatic heart disease requiring valve replacement were selected for study. Ten patients with no cardiac failure, myocardial wall motion abnormalities and myocardial infarction and for whom coronary bypass surgery was planned were selected as the control group. Carnitine levels of myocardial tissue obtained from the right atrium and plasma during the operation were evaluated using spectrophotometric method. Myocardial-free carnitine levels expressed as mumol/g (dry weight) were determined according to Ceberblad and Lindstedt technique.
Myocardial-free carnitine levels in patients were found to be 0.72 +/- 0.37 mumol/g (dry weight) in comparison with 1.44 +/- 1.03 mumol/g (dry weight) in the control group. Myocardial-free carnitine levels in patients were statistically decreased when compared to control group. Plasma-free carnitine levels in patients were 80.91 +/- 28.22 mumol/L and 89.52 +/- 48.21 mumol/L in the control group, respectively. There was no significant difference between plasma-free carnitine levels of the groups.
In our study, myocardial-free carnitine levels were decreased while plasma-free carnitine levels were normal in patient with chronic rheumatic heart disease.
Article: Metabolic cardiology: an integrative strategy in the treatment of congestive heart failure.[show abstract] [hide abstract]
ABSTRACT: Congestive heart failure (CHF) and dilated cardiomyopathy are life-threatening conditions in which the heart muscle is so weak that effective pulsatile action is compromised. Pulmonary vascular congestion and swelling in the lower extremities as well as in the liver and lining of the gastrointestinal tract frequently cause overwhelming symptoms and disability. Millions of Americans suffer from CHF, and more than 500,000 cases are diagnosed annually. Cardiovascular diseases such as hypertension with left ventricular hypertrophy, valvular heart disease, coronary artery disease, myocarditis, and various cardiomyopathies can lead to the progressive onset of CHF. The purpose of this communication article is to introduce metabolic cardiology as a vital therapeutic strategy utilizing nutritional biochemical interventions that preserve and promote adenosine triphosphate (ATP) production. Treatment options that incorporate metabolic interventions targeted to preserve energy substrates (D-ribose) or accelerate ATP turnover (L-carnitine and coenzyme Q10) are indicated for at-risk populations or patients at any stage of CHF. The integration of these metabolic supports provides the missing link in CHF treatment that has been eluding physicians for decades.Alternative therapies in health and medicine 15(3):44-52. · 1.77 Impact Factor