Attenuated early diastolic interventricular septum bulging by pulmonary hypertension due to later developed aortic regurgitation.

A woman was admitted due to dyspnea. She had familial pulmonary arterial hypertension and typical echocardiographic findings including early diastolic bulging of the interventricular septum toward the left ventricular cavity. Her symptoms improved with medication. Five months later, she was hospitalized again due to severe dyspnea. Echocardiography demonstrated aortic valve vegetation and its regurgitation. Echocardiography also showed attenuation of early diastolic compression of the interventricular septum, however, the peak tricuspid regurgitant flow velocity did not improve. It is likely that development of left-sided heart failure attenuated abnormal interventricular septal motion due to pulmonary hypertension.

Effects of valsartan on fibrinolysis in hypertensive patients with metabolic syndrome.

BACKGROUND: The purpose of this study was to analyze the effect of valsartan on abnormal adipocyte metabolism and prothrombotic state in hypertensive patients with metabolic syndrome (MetS). METHODS AND RESULTS: We conducted a multicenter, prospective, randomized, parallel-group controlled trial in 150 hypertensive patients with MetS. They were randomly assigned to receive either 80-160 mg valsartan per day (valsartan group, n=79) or other conventional treatment without a renin-angiotensin system (RAS) inhibitor (non-RAS inhibitor group, n=71). After 1 year, there were no significant differences between the 2 groups in the changes in systolic and diastolic blood pressures (valsartan: 153±15/86±15 to 138±16/77±12 mmHg; non-RAS inhibitor: 150±14/82±15 to 137±15/76±10 mmHg). There was a significant difference in the change in the levels of plasminogen activator inhibitor-1 (PAI-1) between the 2 groups after 1 year (valsartan: 3.7±3.2 ng/ml; non-RAS inhibitor: 5.8±3.3 ng/ml, P=0.04). There was no significant difference between groups in the change in the concentration of adiponectin after 1 year (valsartan: 0.3±0.4 µg/ml; non-RAS inhibitor: 0.9±0.4 µg/ml, P=0.22). The animal study showed aortic PAI-1 protein expression was reduced in double knockout mice of angiotensin II type 1a receptor and apolipoprotein E (apoE) compared with the apoE knockout mice. CONCLUSIONS: Valsartan reduced plasma PAI-1 levels compared to non-RAS inhibitor in hypertensive patients with MetS, which suggests it may be useful for improving fibrinolytic function.

Beneficial effects of Waon therapy on patients with chronic heart failure: results of a prospective multicenter study.

BACKGROUND: We conducted a prospective multicenter case-control study to confirm the clinical efficacy and safety of Waon therapy on chronic heart failure (CHF). METHODS: Patients (n=188) with CHF were treated with standard therapy for at least 1 week, and then were randomized to Waon therapy (n=112) or a control group (n=76). All patients continued conventional treatment for an additional 2 weeks. The Waon therapy group was treated daily with a far infrared-ray dry sauna at 60 degrees C for 15 min and then kept on bed rest with a blanket for 30 min for 2 weeks. Chest radiography, echocardiography, and plasma levels of brain natriuretic peptide (BNP) were measured before and 2 weeks after treatment. RESULTS: NYHA functional class significantly decreased after 2 weeks of treatment in both groups. Chest radiography also showed a significant decrease of the cardiothoracic ratio in both groups (Waon therapy: 57.2+/-8.0% to 55.2+/-8.0%, p<0.0001; control: 57.0+/-7.7% to 56.0+/-7.1%, p<0.05). Echocardiography demonstrated that left ventricular diastolic dimension (LVDd), left atrial dimension (LAD), and ejection fraction (EF) significantly improved in the Waon therapy group (LVDd: 60.6+/-7.6 to 59.1+/-8.4 mm, p<0.0001; LAD: 45.4+/-9.3 mm to 44.1+/-9.4 mm, p<0.05; EF: 31.6+/-10.4% to 34.6+/-10.6%, p<0.0001), but not in the control group (LVDd: 58.4+/-10.3 mm to 57.9+/-10.4 mm; LAD: 46.3+/-9.7 mm to 46.2+/-10.1 mm; EF: 36.6+/-14.1% to 37.3+/-14.0%). The plasma concentration of BNP significantly decreased with Waon therapy, but not in the control group (Waon: 542+/-508 pg/ml to 394+/-410 pg/ml, p<0.001; control: 440+/-377 pg/ml to 358+/-382 pg/ml). CONCLUSION: Waon therapy is safe, improves clinical symptoms and cardiac function, and decreases cardiac size in CHF patients. Waon therapy is an innovative and promising therapy for patients with CHF.

No reflow-like pattern in intramyocardial coronary artery suggests myocardial ischemia in patients with hypertrophic cardiomyopathy.

BACKGROUND AND PURPOSE: To evaluate intramyocardial coronary flow velocity pattern by transthoracic Doppler echocardiography and its clinical significance in patients with hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: In 48 patients with HCM who had angiographically normal coronary artery, coronary flow velocity in the left anterior descending coronary artery (LAD) and intramyocardial coronary artery (IMCA) derived from LAD were evaluated using transthoracic Doppler echocardiography. Two clearly different flow patterns in the IMCA were observed in patients with HCM. Twenty-seven HCM patients (group A) had slow deceleration slope in the IMCA flow (average diastolic deceleration time, 989+/-338; range, 585-1680) and the remaining 21 patients (group B) had steep deceleration slope with diastolic deceleration time <300 ms, resulting in a no reflow-like pattern in the IMCA flow (average diastolic deceleration time, 166+/-67; range, 55-280). There were no significant differences in the clinical characteristics and LAD flow velocity profiles between the two groups. The incidence of cardiovascular symptoms (chest pain or syncope) was significantly higher in group B than in group A (67% vs. 26%, p<0.01). Additionally, exercise-induced ischemia as detected by thallium-201 scintigraphy was significantly more frequent in group B than in group A (6 of 9 (67%) vs. 0 of 9 (0%), p<0.01). CONCLUSIONS: Two different intramyocardial coronary flow velocity patterns are observed in patients with HCM using transthoracic Doppler echocardiography. No reflow-like pattern in the IMCA is strongly related to myocardial ischemia in the absence of epicardial coronary artery stenosis, suggesting that coronary microvascular dysfunction may be a causative mechanism.

A new predictor of improvement in regional left ventricular function assessed by ST/HR slope derived from ST elevation on exercise testing in patients with healed myocardial infarction.

This study evaluates the clinical usefulness of ST/HR slope derived from ST elevation on exercise to predict the improvement in regional wall motion following coronary revascularization in patients with healed myocardial infarction. We studied 58 patients with a diseased, infarct-related and single-vessel coronary artery. The decline calculated from the final 12 data points relating ST-segment elevation to heart rate during exercise were derived (ST/HR slope). Hypokinesis in the infarcted region was assessed by the centerline method and expressed in terms of standard deviations (SD/chord). The increase more than 30% of the SD/chord, which was defined as the improvement in regional wall motion, was seen in 23 of the 30 patients with a ST/HR slope of > or = 5.0 (microV/bpm), and in 4 of the 28 patients with a ST/HR slope <5.0 (microV/bpm) (P <.0001). Thus, a ST/HR slope derived from ST elevation on exercise identifies subgroups of patients who show a good recovery of regional wall motion.