Previous studies using pulsed Doppler echocardiography have demonstrated a pattern of abnormal left ventricular relaxation associated with increasing age. Specifically, aging is associated with decreased peak velocity of early diastolic mitral inflow, increased peak velocity of late diastolic inflow, increased isovolumic relaxation time, and early diastolic deceleration time. Abnormal relaxation can progress to significantly elevated left atrial pressure--characterized by increased early peak velocity and shortened isovolumic relaxation time and deceleration time--as part of the disease processes. Left ventricular diastolic dysfunction is highly prevalent, occurring in one half to two thirds of elderly patients with congestive heart failure, in association with normal systolic function. Left ventricular hypertrophy, which is commonly related to systemic arterial hypertension, and ischemic heart disease are the two major causes of abnormal left ventricular diastolic function in the elderly. Recently, newer echocardiographic techniques have been described that allow more accurate evaluation of left ventricular diastolic function. Treatments for left ventricular diastolic dysfunction should focus on the underlying disease etiology as well as on the derangement in left ventricular diastolic function. Although calcium channel blockers and angiotensin-converting enzyme inhibitors have been used clinically to treat diastolic dysfunction, their effects on prognosis remain unproven.
oronary arteriovenous fistula (CAVF) is an abnormal communication between a coronary artery and a cardiac chamber, great vessel, or other vascular structure. Most of them are found incidentally during coronary angiography (CAG), and are identified as a cause of a continuous murmur, myocardial ischemia, congestive heart failure or, rarely, bacterial endocarditis. [1][2][3] However, cases with pericardial effusion (PE) caused by rupture of the aneurysmal coronary artery are quite rare; only 3 cases of cardiac tamponade caused by rupture of the CAVF have been previously reported. [4][5][6] We report a case of chronic PE caused by a CAVF. The PE was observed for 6 months, and finally developed into cardiac tamponade. Case ReportA 75-year-old woman was referred to hospital for investigation of recurrent PE. She had a history of pulmonary tuberculosis 50 years ago. In August 1998, she had been admitted to another hospital for further investigation of cardiomegaly (cardiothoracic ratio (CTR) 63%) and was the PE was diagnosed for the first time. However, she was free of symptoms and the laboratory examinations were normal, including thyroid function and tuberculin reaction. Chest computed tomography (CT) did not show any abnormal findings except for the PE and a scar from the pulmonary tuberculosis. She was treated with diuretics and the PE disappeared within 6 months. The CTR decreased Circulation Journal Vol.66, August 2002from 63% to 54% on the chest X-ray. In February 1999, she developed shortness of breath and general fatigue, and echocardiographic examination revealed that the PE had recurred.On the admission to hospital in February 1999, her vital signs were: blood pressure 148/70 mmHg, heart rate 92 beats/min, respiratory rate 20 breaths/min, and body temperature 36.5°C. Pulsus paradoxus was not detected. Chest auscultation revealed bilaterally normal respiratory sounds and a soft continuous murmur at the left sternal border of the 4th intercostal space. She had hepatomegaly, bilateral leg edema and a markedly expanded external jugular vein.Laboratory tests were as follows: leukocytes 7.2×10 3 / l; C-reactive protein 0.5 mg/dl; erythrocyte sedimentation rate of 24 mm/h; TSH 1.86 IU/ml; free T3 1.77 pg/ml; free T4 0.83 ng/ml; tuberculin reaction 10×10 mm. A chest Xray revealed cardiomegaly (CTR = 67%) without pulmonary infiltration. The electrocardiogram (ECG) on admission was normal except for flat T waves in leads V4-6 (Fig 1A). An enhanced CT scan revealed a dilated right coronary artery (RCA) and a dilated coronary sinus (CS) vein, an expanded inferior vena cava and a large, circumferential PE (Fig 2). However, leakage of contrast media into the pericardial space was not seen. A diagnostic pericardiocentesis yielded 20 ml of bloody fluid (Hct = 22%) that contained 5.7 mg/dl of protein, 56 mg/dl of glucose and 23.2 IU/L of adenosine deaminase. The culture for bacteria in the pericardial fluid was negative, and a polymerase chain reaction for the tuberculosis bacillus was not detected. There was no evidence of ...
Hypertrophic cardiomyopathy (HCM) is a rare cardiac complication in patients with Klinefelter syndrome. We report the case of a 67-year-old Japanese man with Klinefelter syndrome, HCM, sick sinus syndrome, and coronary arteriovenous fistula, in whom the 47XXY/46XY mosaic pattern was revealed by chromosomal study. Echocardiography revealed HCM with an interventricular septum thickness of 17 mm and a left ventricular posterior wall thickness of 10 mm. Sick sinus syndrome type III was diagnosed by paroxysmal atrial fibrillation (longest sinus arrest 9.0 sec) on 24-h Holter ECG recording. Coronary arteriovenous fistula was detected from the left anterior descending artery to the right ventricle by coronary arteriography. To our knowledge, this is the first case report of Klinefelter syndrome with HCM. As there have been a few reports of patients with Klinefelter syndrome in association with skeletal muscular diseases such as Becker-type muscular dystrophy or myotonic dystrophy, the gene mutation that causes Klinefelter syndrome may occur in the cardiac muscle. HCM may represent another variable expression of this chromosomal abnormality.
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