Case report: Dual atrioventricular nodal non-reentrant tachycardia with six types of ECG patterns leading to tachycardia-induced cardiomyopathy in a 51-year-old man.

More than three types of ECG manifestations in one patient with dual atrioventricular nodal non-reentrant tachycardia (DAVNNT) are rare. We report a 51-year-old male patient with DAVNNT consisting of six types of ECG patterns leading to tachycardia-induced cardiomyopathy. After radiofrequency ablation of the slow pathway, DAVNNT was eliminated and cardiac function was restored.

Acute Myocardial Infarction in a Young Man with Hyperhomocysteinemia and Pulmonary Tuberculosis.

Acute myocardial infarction, hyperhomocysteinemia and pulmonary tuberculosis (PTB) are rare in individuals under the age of 30 years. We herein report the case of a 27-year-old man who presented with intermittent chest pain, elevated homosysteine level, and PTB. The patient was treated successfully with a combination of medications and percutaneous coronary intervention. This uncommon case highlights that homocysteine, folate and B vitamins levels should be regularly evaluated, and that chest X-rays or thoracic computed tomography should be ordered routinely to exclude PTB in patients under the age of 30 years who present acute myocardial infarction and lack the traditional risk factors.

The role of TWEAK/Fn14 in cardiac remodeling.

The pathophysiological basis of heart failure is cardiac remodeling, a process that comprises structural and functional changes including cardiomyocyte proliferation, hypertrophy, necrosis, apoptosis, autophagy, interstitial fibrosis, contractile dysfunction and ventricular dilatation. Accumulating evidence demonstrate that tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is involved in the process by binding its receptor fibroblast growth factor-inducible molecule 14 (Fn14). In this review, we will discuss the potential role of the TWEAK/Fn14 axis in cardiac remodeling, elucidate its possible mechanisms and explore new therapeutic targets for heart failure.

TWEAK/Fn14 promotes the proliferation and collagen synthesis of rat cardiac fibroblasts via the NF-кB pathway.

We wished to elucidate a potential role of the tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible molecule 14 (Fn14) axis in myocardial fibrosis. Stimulation of neonatal rat cardiac fibroblasts (CFs) with TWEAK could increase CFs numbers and collagen synthesis. Conversely, when CFs were pretreated with siRNA against Fn14, induction of cell proliferation and collagen synthesis by TWEAK were inhibited. Pretreatment with TWEAK on CFs induced activation of the nuclear factor-kappaB (NF-кB) pathway and subsequently increased the production of metalloproteinase-9 (MMP-9). Cell treatment with siRNA against Fn14 led to inhibition of the NF-кB pathway. Additionally, after stimulation of cell with ammonium pyrrolidine dithiocarbamate, cell proliferation and collagen synthesis induced by NF-кB and the upregulation of MMP-9 production were inhibited. The present study suggested that the TWEAK/Fn14 axis increased cell proliferation and collagen synthesis by activating the NF-кB pathway and increasing MMP-9 activity. This axis may be important for regulating myocardial fibrosis.

Increased plasma osteoprotegerin levels are associated with the presence and severity of acute coronary syndrome.

OBJECTIVE: The objective of this study was to explore the relationship between increased plasma osteoprotegerin (OPG) levels and acute coronary syndrome (ACS). METHODS: Plasma OPG levels from 85 subjects undergoing coronary artery angiography in three different groups, including ACS (n=45), stable angia pectoris (SAP) (n=20) and normal coronary artery (NCA) (n=20), were detected by ELISA. Twenty-two ascending aorta specimens were surgically taken from 8 ACS, 7 SAP and 7 NCA patients, and OPG mRNA expression in the specimens was detected by RT-PCR. In addition, 10 coronary artery sections each were selected from autopsy archives for the presence of vulnerable atherosclerosis plaques (VP), stable plaques (SP) or no plaques (NP) and OPG protein expression in the sections was detected by immunohistochemistry. RESULTS: Plasma OPG concentrations in the ACS group were significantly higher than those in the SAP or NCA group.The levels of plasma OPG in the 1-, 2- and 3-vessel disease subgroups of ACS were increasingly higher (P < 0.05 or 0.01). Multiple logistic regression analyses revealed a significant independent relation between plasma OPG concentration and the presence of ACS (P = 0.032, odd ratio = 1.006).Ascending aorta specimens from the ACS group had a greater OPG mRNA expression than those from the NCA or SAP group (P < 0.01). Sections with VP had a markedly higher OPG expression than sections with SP or NP (P < 0.05 and P < 0.01, respectively). CONCLUSIONS: Increased plasma osteoprotegerin levels are associated with the presence and severity of acute coronary syndrome.

A high association of aortic valve sclerosis detected by transthoracic echocardiography with coronary arteriosclerosis.

OBJECTIVE: To examine whether aortic valve sclerosis (AVS) detected by transthoracic echocardiography (TTE) has a high association with coronary arteriosclerosis. METHODS: Clinical and angiographic features and TTE findings were retrospectively analyzed in a blinded fashion for 138 consecutive patients, of whom 58 had AVS and 80 had non-AVS diseases. Both histological and immunohistochemical studies were performed on frozen aortic valve sections obtained at autopsy from 7 AVS and 3 non-AVS patients. RESULTS: AVS and coronary artery disease (CAD) had similar clinical risk factors. The AVS group had a higher positive rate of coronary angiography and a higher incidence rate of multivessel CAD than the non-AVS group. The sensitivity, specificity, positive predictive value and negative predictive value of AVS in diagnosing CAD were 63.8, 71.3, 61.7 and 73.1%, respectively. Early lesions of AVS were characterized by accumulation of lipid and infiltration of macrophages and T lymphocytes as indicated by immunohistochemical staining. Late lesions were characterized by formation of calcific plaques, proliferation of fibrous connective tissue and immunohistochemical staining identifying a few macrophages or T lymphocytes and little lipid accumulation on the surface of aortic valve leaflets. Late lesions in the basement of aortic valve leaflets were characterized by hyperplastic granulation tissues. Three aortic valve leaflets from the non-AVS group were characterized by nonspecific thickened tips, increased collagen, no calcification, no lipid accumulation and no inflammatory cells. CONCLUSIONS: There were significant similarities in clinical risk factors, histopathological alterations of AVS and coronary atherosclerosis. AVS detected by TTE had a high association with coronary arteriosclerosis.