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Background Ghrelin is a novel growth hormone (GH)-releasing peptide, isolated from the stomach, that may also cause a positive energy balance by stimulating food intake and inducing adiposity. We sought to investigate the pathophysiology of ghrelin in the cachexia associated with chronic heart failure (CHF). Methods and Results Plasma ghrelin was measured in 74 patients with CHF and 12 control subjects, together with potentially important anabolic and catabolic factors, such as GH and tumor necrosis factor (TNF-α). Patients with CHF were divided into two groups, those with cachexia (n=28) and those without cachexia (n=46). Plasma ghrelin did not significantly differ between all CHF patients and controls (181±10 versus 140±14 fmol/mL, P =NS). However, plasma ghrelin was significantly higher in CHF patients with cachexia than in those without cachexia (237±18 versus 147±10 fmol/mL, P r =0.28, P r =0.31, P r =−0.35, P Conclusions Plasma ghrelin was elevated in cachectic patients with CHF, associated with increases in GH and TNF-α and a decrease in body mass index. Considering ghrelin-induced positive energy effects, increased ghrelin may represent a compensatory mechanism under catabolic-anabolic imbalance in cachectic patients with CHF.

Background Atherosclerotic change in the coronary artery is associated with an impaired vessel wall distensibility. However, there are few data regarding the relation between vessel wall morphology and distensibility. Therefore, with intravascular ultrasound, we assessed coronary artery distensibility in angiographically normal coronary segments of humans. Methods and Results Data were analyzed at 35 angiographically normal coronary sites where circumferential or noncircumferential lesions were demonstrated by ultrasound in 22 patients (mean age, 55 years). After intracoronary injection of 500 μg nitroglycerin (NTG), coronary luminal area was measured with intravascular ultrasound (30 MHz, 3.5F to 4.3F, 1800 rpm). Intracoronary pressure was simultaneously measured with a 2F micromanometer-tipped catheter located at the left main coronary artery. The coronary distensibility index was calculated as 10-fold the ratio of luminal area change to intracoronary pressure change during a cardiac cycle. Another pressure-independent vascular stiffness index, β, was derived by the following formula: β=[ln(SBP/DBP)]/(dD/diastolic mean diameter), where SBP is systolic intracoronary pressure, DBP is diastolic intracoronary pressure, and dD is the difference between systolic and diastolic diameters. At the sites where luminal areas were measured, thickness of intima-media complex, defined as the distance between the intimal leading edge and the adventitial leading edge, was determined as an index of the severity of atherosclerosis. In seven segments, distensibility index was determined before and after NTG injection to examine the effect of NTG on coronary distensibility. In all examined sites, including circumferential and noncircumferential lesions, the luminal area was 12.6±5.0 mm 2 during systole and 11.6±4.6 mm 2 during diastole, and the calculated coronary distensibility index ranged from 0 to 0.83 mm 2 /mm Hg. The thickness of the intima-media complex ranged from 0.12 to 1.30 mm, suggesting the presence of various grades of atherosclerosis even in the absence of angiographic lesions. There was a poor inverse correlation between thickness of the intima-media complex and distensibility index ( r =.19, y =−0.17 x +0.41, P =.29). However, when noncircumferential lesions were excluded for evaluation, there was a significant inverse correlation between them ( r =.58, y =−0.50 x +0.72, P −1 ), which ranged from 0.28 to 3.99 ( r =.70). After NTG injection, coronary distensibility increased by an average of 71% in the segments with a thin intima-media complex, whereas it did not substantially change in those with a relatively thick intima-media complex. Conclusions These results suggest that coronary distensibility is impaired in the coronary sites accompanying occult atherosclerosis, none of which can be detected by the conventional angiography. NTG can augment coronary distensibility in the segments without a markedly thickened intima-media complex. We suggest that thickness of the intima-media complex can contribute to determining the coronary distensibility in clinical settings.

Pulmonary arterial hypertension, pulmonary veno-occlusive disease, and pulmonary capillary hemangiomatosis are included in the same group (group 1) of clinical classification of pulmonary hypertension.1 Histological changes in the small pulmonary arteries (ie, intimal fibrosis and medial hypertrophy) are similar in these 3 diseases, and clinical presentations of the 3 diseases are often indistinguishable.1 However, it is estimated that the hemodynamics of capillary vessels are quite different in each disease. The hemodynamics of capillary vessels (ie, capillary occlusion) play an important role in cardiovascular diseases.2 Thus, clarification of the differences in the hemodynamics is essential to understand the pathophysiology of these 3 diseases. We obtained lung segments from patients with pulmonary hypertension who underwent living-donor lung transplantation and from patients with …

BACKGROUND The signal-averaged ECG has been used to detect late potentials, and it is considered a noninvasive marker for areas of slow conduction requisite for reentrant arrhythmia. Late potentials are not usually found in patients with idiopathic ventricular tachycardia (VT); nevertheless, fragmented electrograms are often recorded in those patients during endocardial mapping. The purpose of this study was to investigate the spectral content of the signal-averaged ECGs with use of fast Fourier transform analysis (FFT) in patients with idiopathic VT of left ventricular origin. METHODS AND RESULTS Signal-averaged ECGs were recorded in 12 patients with idiopathic VT originating from the left ventricle (group 1) and 25 age-matched normal volunteers (group 2). Frequency analysis with FFT was performed with a Blackman-Harris window in a segment length of 120 msec from 40 msec before the end of the QRS complex, and the frequency spectrum was displayed in a three-dimensional graph. Area ratio 1 (area of 20-50 Hz/area of 10-50 Hz) and area ratio 2 (area of 40-100 Hz/area of 0-40 Hz) were calculated in all subjects. Late potentials defined by the time domain were negative in all subjects. The area ratios of group 1 were significantly higher than those of group 2. High-frequency components in the three-dimensional graph were confined within the QRS complex. CONCLUSIONS These results suggest that frequency analysis of signal-averaged ECGs with FFT is an available method for detecting the high-frequency component within the QRS complex in some patients with idiopathic VT of left ventricular origin.

Patients with hypertrophic cardiomyopathy sometimes develop extreme hypertrophy in the left ventricle. A 78-year-old woman showed rapid progression of left ventricular hypertrophy. She was referred to our hospital at the age of 73 years because of left ventricular hypertrophy on seen on ECG. …

Background— Infusion of adrenomedullin (AM) has beneficial hemodynamic effects in patients with heart failure. However, the effect of AM on myocardial ischemia/reperfusion remains unknown. Methods and Results— Male Sprague-Dawley rats were exposed to a 30-minute period of ischemia induced by ligation of the left coronary artery. They were randomized to receive AM, AM plus wortmannin (a phosphatidylinositol 3-kinase [PI3K] inhibitor), or saline for 60 minutes after coronary ligation. Hemodynamics and infarct size were examined 24 hours after reperfusion. Myocardial apoptosis was also examined 6 hours after reperfusion. The effect of AM on Akt phosphorylation in cardiac tissues was examined by Western blotting. Intravenous administration of AM significantly reduced myocardial infarct size (28±4% to 16±1%, P P P Conclusions— Short-term infusion of AM significantly attenuated myocardial ischemia/reperfusion injury. These cardioprotective effects are attributed mainly to antiapoptotic effects of AM via a PI3K/Akt-dependent pathway.

Background —Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by local or diffuse wall motion abnormalities in the right ventricle (RV), associated with recurrent ventricular tachycardia (VT) of RV origin. Brain natriuretic peptide (BNP) was first isolated from a porcine brain extract. In humans, BNP is expressed predominantly in the ventricles of failing hearts, and its expression has been observed primarily in myocytes in the interstitial fibrous area in dilated cardiomyopathy. We hypothesized that BNP is increasingly secreted from the residual myocytes within the atrophic tissue in patients with ARVD. Methods and Results —Plasma BNP levels were measured in 17 patients with ARVD, 12 patients with idiopathic RV outflow tract tachycardia (RVOT), and 120 control subjects. We performed cardiac catheterization, RV endomyocardial biopsy, electron- beam CT, and biventricular endomyocardial mapping in the ARVD patients. There was a significant increase in plasma BNP levels in the ARVD patients compared with the RVOT patients and control subjects (61.4±59.6 pg/mL versus 8.3±5.5 pg/mL and 9.3±5.8 pg/mL; P r =−0.588, P =0.025) and with the fractionated-area scores ( r =0.705, P =0.005). Light microscopic immunohistochemistry showed strong BNP immunoreactivity in residual myocytes with fibrofatty replacement. Conclusions —These results suggest that plasma BNP levels were not increased in RVOT patients but were increased in ARVD patients, and that the increased BNP levels indicate the severity of both the RV dysfunction and the arrhythmogenic substrate.

A 30-year-old woman was referred to our clinic because of shortness of breath and general fatigue. She had been well until 2 months earlier, when she noticed mild shortness of breath during and after exercise. Physical examination revealed a systolic heart murmur at the left parasternal area. Transthoracic echocardiography demonstrated an abnormal mass located just proximal to the pulmonary valve occupying the right ventricular outflow tract (Figure 1⇓, top left). …