n essential hypertension, changes in the morphology of the left ventricle (LV) are commonly observed, and are considered to be the result of adaptation to pressure overload. The changes have been classified into 4 geometric patterns based on the LV mass and wall thickness. 1 These geometric changes are consistent with progression of heart failure in an experimental model, 2 and furthermore, are considered to reflect the course of hypertensive heart failure. 3,4 On the other hand, it has been speculated that a disorder of myocardial energetic metabolism relates to progression of heart failure. 123 I-15-p-iodophenyl-3-(R,S)-methylpentadecanoic acid (I-123 BMIPP) is a radioisotope used for assessment of myocardial free fatty acid (FFA) metabolism and abnormal myocardial uptake of BMIPP has been reported in patients with heart failure. 13 However, Japanese Circulation Journal Vol.65, September 2001 it has not been clarified whether the pathophysiological adaptation of changing the LV morphology in hypertensive hearts is related to changes in myocardial FFA metabolism. MethodsThirty-five patients (21 men, 14 women; mean age: 61±11 years) who had a history of essential hypertension (blood pressure ≥160 mmHg at systole or 90 mmHg at diastole according to the WHO criteria) were enrolled. The patients were free of any symptoms of ischemic heart disease, valvular heart disease, or concomitant important diseases such as diabetes mellitus. Two patients with symptomatic congestive heart failure (New York Heart Association class II-III) who took some diuretics were included. The evaluations, including a detailed medical history, 12-lead ECG, urinalysis, and serum levels of urea nitrogen, creatinine, glucose, cholesterol, sodium, potassium and calcium, were performed in all subjects. An echocardiogram of adequate quality to assess LV morphologic characteristics was also obtained from all subjects. Patients who showed LV asymmetrical hypertrophy on the echocardiogram were excluded, as were patients with diabetes mellitus or renal failure. All patients in the study gave written informed consent.Echocardiography was performed using an ultrasonic sector scanner with 2.5-and 3.75-MHz transducers (SONOLAYER SSH-160A Toshiba Co, Japan The left ventricle's morphological adaptation to high blood pressure is classified into 4 patterns based on mass and wall thickness. The geometric changes caused by maladaptation to pressure overload possibly relate to progression of contractile dysfunction with abnormal energy metabolism. The present study assessed whether the geometric adaptation of the left ventricle (LV) to high blood pressure relates to changes in myocardial energy metabolism, especially free fatty acid (FFA) utilization. Thirty-five patients with essential hypertension underwent echocardiography and dual isotopes myocardial scintigraphy using iodine-123 labeled 15-p-iodophenyl-3-(R,S)-methylpentadecanoic acid (BMIPP, an analogue of a FFA) and . Systolic (endocardial fractional shortening; %FS) and diastolic indices (the ratio o...
Adenosine triphosphate (ATP) is reported to be released mainly from presynaptic vesicles and cardiomyocytes. The released ATP, which can be degraded to adenosine, may cause coronary vasodilation. However, there is no clear evidence that ATP is degraded to adenosine and causes coronary vasodilation in humans. The present study was undertaken to test whether intracoronary administration of ATP increases myocardial adenosine levels and coronary blood flow. In 11 patients, 3 doses of ATP (0.1, 0.2, and 0.4 mg) were injected into the left anterior descending coronary artery. The velocity of coronary blood flow was measured by Doppler flow probe, and the adenosine concentration in the coronary sinus blood was measured. We also continuously infused ATP (0.2 mg/min) for 1 min in another 10 patients. Coronary blood flow increased dose dependently soon after injection of ATP. Coronary arteriovenous differences in adenosine concentration increased [from 21 +/- 15 to 178 +/- 15 pmol/ml (p < 0.05) 10 sec after the injection of ATP (0.4 mg)] and there were marked reductions in both aortic blood pressure and heart rate. The adenosine levels returned to baseline 20 sec after the injection of ATP, and aortic blood pressure and heart rate also recovered, although coronary blood flow remained increased. Furthermore, continuous infusion of ATP for 1 min increased coronary blood flow velocity and coronary arteriovenous differences in adenosine concentration from 25 +/- 14 to 71 +/- 13 pmol/ml (p < 0.05) in 10 patients. These results indicate that intracoronary administration of ATP immediately increases coronary blood flow and the adenosine concentration of coronary venous blood, which returns to the baseline level thereafter. The differences in the time courses of increases in coronary venous adenosine levels and coronary blood flow after ATP injections suggest that vasodilatory mechanisms other than adenosine, eg, nitric oxide and prostaglandins, may also be involved in the ATP-induced coronary vasodilation. ATP may be used as a cardioprotective agent as well as adenosine.
Our findings suggest that impairment of myocardial FFA metabolism rather than small vessel abnormalities in the myocardium is responsible for modest left ventricular dysfunction in patients with diabetes.
We report a case of hypertensive-diabetic cardiomyopathy demonstrating left ventricular regional wall motion abnormality, with a normal coronary artery documented on coronary arteriography. Dipyridamole-infusion 201Tl scintigraphy demonstrated transient perfusion defects in the infero-posterior wall of the left ventricle, where reduced wall motion was demonstrated on contrast left ventriculography. Myocardial SPECT (single photon emission tomography) imaging with [123I] beta-methyliodophenylpentadecanoic acid (BMIPP) and 201Tl demonstrated reduced [123I]BMIPP uptake compared with 201Tl uptake in the infero-posterior wall of left ventricle. These results suggest that the impairment of myocardial free fatty acid metabolism is an etiologic or contributory factor for regional wall motion abnormality, together with small-vessel coronary artery disease, in this patient.
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