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With the exception of contrast-enhanced cardiovascular magnetic resonance imaging, clear distinction of takotsubo cardiomyopathy from anterior wall myocardial infarction cannot be achieved currently by simple and noninvasive tests. The aim of this study was to examine the role of inferior ECG leads in distinguishing these two conditions. From January 2004 to June 2006, eight female patients suffering from takotsubo cardiomyopathy were identified by the Mayo Clinic criteria. The clinical and ECG features were compared with 27 consecutive sex- and age-matched patients with anterior wall myocardial infarction admitted to the Coronary Care Unit within the same period. The observed ECG features were then verified with that of 62 published cases of takotsubo cardiomyopathy. Takotsubo cardiomyopathy patients had similar left ventricular ejection fraction (35.0% ± 5.7% vs 38.2% ± 6.4%, P = 0.829), lower peak creatinine kinase level (461 ± 330 U/l vs 2723 ± 1826 U/l, P = 0.020), more ST-segment elevation in the inferior leads (50% vs 7.4%, P = 0.016), and virtually no ST-segment depression in inferior leads (0% vs 48.2%, P = 0.015) compared with patients who had anterior wall myocardial infarction. ST-segment elevation of ≥1.0 mm in lead II had 62.5% sensitivity and 92.6% specificity in detecting takotsubo cardiomyopathy. The observed ECG characteristics were comparable with those in the literature. In patients who present with anterior wall myocardial infarction, the absence of ST-segment depression or ST-segment elevation in inferior leads, especially if the ST-segment in lead II ≥ III, is highly suggestive of takotsubo cardiomyopathy.

We studied the chronic effects of chlorpromazine (CPZ) on the myocardium of rats using light and electron microscopy. Wistar strain rats were divided into two groups and given either normal saline or CPZ intraperitoneally at a dose of 5 mg/kg body weight/day for 30 consecutive days. Myocardial degeneration, atrophic muscle fiber, and myocardial fibrosis were observed by light microscopy in all CPZ-treated rats. Ultrastructural alterations of the myocardium were also found in all CPZ-treated rats. They consisted of contracted myofibers, mitochondriosis, degenerated mitochondria, dilated sarcoplasmic reticulum, and increased collagen fibers. However, no abnormal histologic or ultrastructural changes were observed in the normal saline-treated rats. We therefore conclude that a chronic administration of a sedative dose of CPZ causes myocardial damage in rats.

Persistent left superior vena cava (PLSVC) is a rare congenital anomaly whose prevalence is 0.3 % of general population. The majority of PLSVC drain into right atrium (RA) through the coronary sinus without clinical harm. However, in about 10 % of patients with PLSVC, it drains into left atrium (LA) causing right-to-left shunt. Here, we present a 60-year-old male patient with a PLSVC draining into LA, who developed dyspnea and desaturation depending on the body position after trans-catheter coil embolization of coronary to pulmonary artery fistulas. PLSVC draining into LA should be included in the differential diagnosis of positional desaturation.

The aim of this study was to investigate the regulation mechanism of aquaporin 9 (AQP9) gene on inflammatory response and cardiac function in rats with myocardial infarction (MI) through extracellular signal-regulated kinase1/2 (ERK1/2) pathway. The constructed rats models of MI were randomly divided into 6 groups: control group (sham operation group, MI modeling sham operation), model group (MI modeling), NC group (MI modeling, tail vein injection of AQP9 negative control sequence vector), AQP9 shRNA group (MI modeling, tail vein injection of AQP9 shRNA plasmid vector), U0126 group (MI modeling, tail vein injection of ERK signaling pathway inhibitor), and AQP9 shRNA + U0126 group. The hemodynamics and cardiac function of rats in each group were detected on the seventh day of modeling. The levels of AQP9 and inflammatory factors [tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-10 (IL-10)] in peripheral blood of rats were detected by ELISA method. qRT-PCR and western blot were used to detect the mRNA and protein expression of AQP9, ERK1/2, B-cell lymphoma-2 (Bcl-2), Bcl-associated x (Bax) in the myocardial tissue of rats. TTC and TUNEL staining were used to observe myocardial infarct size and apoptosis of myocardial cells in each group. Compared with control group, the levels of heart rate, left ventricular end-diastolic pressure, TNF-α, and IL-6 were increased in each group of rats with MI (all p < 0.05), while the levels of systolic blood pressure, diastolic blood pressure, mean arterial pressure, left ventricular systolic pressure, and IL-10 were significantly decreased (all p < 0.05). The mRNA and protein expression levels of AQP9, ERK1/2 phosphorylation and Bax were significantly increased, as well as the myocardial infarct size, apoptosis index of myocardial tissue (all p < 0.05), the mRNA and protein expression levels of Bcl-2 were significantly decreased (all p < 0.05). The AQP9 gene knock-down or exogenous administration of the ERK1/2 inhibitor U0126 could improve the above indexes. However, the combination of AQP9 gene knock-down and U0126 showed no further effect. Silencing AQP9 gene can inhibit the activation of ERK1/2 signaling pathway, attenuate the inflammatory response in rats with MI, inhibit apoptosis of myocardial cells, and improve cardiac function.

Regional hemodynamic responses to the vasodilators, hydralazine (1mg/kg, i.v.) and verapamil (0.1 mg/kg/min, i.v.), were examined in conscious Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), 15 and 50 weeks of age, using the radioactive microsphere method. The flow rates of heart and skeletal muscle in SHR were higher than those in WKY, and the flow rates of liver, kidney, intestines, and skin in SHR were lower than those in WKY. These differences between the regional blood flow in WKY and SHR were observed in both aged and young rats. The changes in organ blood flow induced by hydralazine and verapamil were similar for WKY and SHR in most organs. Both drugs increased the skeletal muscle blood flow in WKY and young SHR, but not in aged SHR, that is, the skeletal muscle blood vessels in aged SHR lost their vasodilatory response. These results suggest that, although a lack of vasodilatory responses in the skeletal muscle vasculature of aged SHR may be triggered by persistent hypertension, the vital organ vasculature maintains its normal vasodilating capacity.

Conventional therapy of patients with idiopathic dilated cardiomyopathy is currently directed at the control of heart failure. However, the morbidity and mortality of idiopathic dilated cardiomyopathy remains very high despite such interventions. One promising new approach to therapy of idiopathic dilated cardiomyopathy is β-blockade. The potential mechanisms for benefit from β-blockade include protection from catecholamine cardiotoxicity, upregulation of myocardial β-adrenergic receptors, reduction in sudden death, reduction in heart rate, improved ventricular diastolic function, and reduction in afterload. Several reports have suggested that longterm β-blockade may improve hemodynamic function, clinical symptoms, and survival in patients with idiopathic dilated cardiomyopathy. However, data from controlled trials are limited and some reports have been negative. This paper will summarize the rationale for the use of β-blocker therapy in idiopathic dilated cardiomyopathy and review the clinical experience with this therapy.