Pulmonary artery catheterization in acute myocardial infarction complicated by cardiogenic shock: A review of contemporary literature.

Acute myocardial infarction (AMI) with left ventricular (LV) dysfunction patients, the most common cause of cardiogenic shock (CS), have acutely deteriorating hemodynamic status. The frequent use of vasopressor and inotropic pharmacologic interventions along with mechanical circulatory support (MCS) in these patients necessitates invasive hemodynamic monitoring. After the pivotal Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness trial failed to show a significant improvement in clinical outcomes in shock patients managed with a pulmonary artery catheter (PAC), the use of PAC has become less popular in clinical practice. In this review, we summarize currently available literature to summarize the indications, clinical relevance, and recommendations for use of PAC in the setting of AMI-CS.

Comparison of percutaneous device closure versus surgical closure of peri-membranous ventricular septal defects: A systematic review and meta-analysis.

BACKGROUND: While percutaneous device closure (PDC) is a first-line therapy for isolated muscular ventricular septal defects (mVSD), surgery is still the preferred approach for peri-membranous ventricular septal defects (pmVSD). OBJECTIVE: We sought to compare the outcomes of percutaneous versus open surgical closure of pmVSDs. METHODS: PubMed, Cochrane Library, and Web of Science databases were searched through October 15, 2014 for English language studies comparing outcomes of PDC with surgical closure of pmVSDs. Study quality, publication bias, and heterogeneity were assessed. A meta-analysis of selected studies was performed using a random effects model. Comparison was done for early (<1 month) safety and efficacy outcomes. RESULTS: Seven studies with a total of 3,134 patients (PDC = 1,312, surgery = 1,822) were identified. Patients in the PDC group were older than those treated surgically (mean age 12.2 vs. 5.5 years, respectively). In six out of seven studies, the mean VSD size was found to be comparable between the treatment arms (PDC 4.9 mm vs. surgery 6.0 mm). Males represented 52% of patients in either group. Follow-up ranged from 5 to 42 months. No significant differences were observed between PDC vs. surgery in terms of procedural success rate [relative risk (RR): 1.00, confidence interval (CI): 0.99-1.00; P = 0.67]. Combined safety end points for major complications (early death/reoperation/permanent pacemaker) were similar in both groups (RR: 0.55, CI: 0.23-1.35; P = 0.19) as were as other outcomes like post-procedure significant residual shunt (RR: 0.69, CI: 0.29-1.68; P = 0.41), significant valvular (aortic/tricuspid) regurgitation (RR: 0.70, CI: 0.26-1.86; P = 0.47), and advanced heart block (RR: 0.99, CI: 0.46-2.14; P = 0.98). The need for blood transfusion (RR: 0.02, CI: 0.00-0.05; P < 0.001) and duration of hospital stay [standard mean difference (SMD) -2.17 days, CI: -3.12 to -1.23; P < 0.001] were significantly reduced in the PDC group. CONCLUSION: Percutaneous closure of pmVSD when performed in a selected subgroup of patients is associated with similar procedural success rate without increased risk of significant valvular regurgitation or heart block when compared with surgical closure.

Vitamin D deficiency induces cardiac hypertrophy and inflammation in epicardial adipose tissue in hypercholesterolemic swine.

INTRODUCTION: Vitamin D is a sectosteroid that functions through Vitamin D receptor (VDR), a transcription factor, which controls the transcription of many targets genes. Vitamin D deficiency has been linked with cardiovascular diseases, including heart failure and coronary artery disease. Suppressor of cytokine signaling (SOCS)3 regulates different biological processes such as inflammation and cellular differentiation and is an endogenous negative regulator of cardiac hypertrophy. OBJECTIVE: The purpose of this study was to test the hypothesis that vitamin D deficiency causes cardiomyocyte hypertrophy and increased proinflammatory profile in epicardial adipose tissue (EAT), and this correlates with decreased expression of SOCS3 in cardiomyocytes and EAT. METHODS: Eight female Yucatan miniswine were fed vitamin D-sufficient (900 IU/d) or vitamin D-deficient hypercholesterolemic diet. Lipid profile, metabolic panel, and serum 25(OH)D levels were regularly measured. After 12 months animals were euthanized and histological, immunohistochemical and qPCR studies were performed on myocardium and epicardial fat. RESULTS: Histological studies showed cardiac hypertrophy, as judged by cardiac myocyte cross sectional area, in the vitamin D-deficient group. Immunohistochemical and qPCR analyses showed significantly decreased mRNA and protein expression of VDR and SOCS3 in cardiomyocytes of vitamin D-deficient animals. EAT from vitamin D-deficient group had significantly higher expression of TNF-α, IL-6, MCP-1, and decreased adiponectin in association with increased inflammatory cellular infiltrate. Interestingly, EAT from vitamin D-deficient group had significantly decreased expression of SOCS3. CONCLUSION: These data suggest that vitamin D deficiency induces hypertrophy in cardiomyocytes which is associated with decreased expression of VDR and SOCS3. Vitamin D deficiency is also associated with increased inflammatory markers in EAT. Activity of VDR in the body is controlled through regulation of vitamin D metabolites. Therefore, restoration of VDR function by supplementation of VDR ligands in vitamin D-deficient population might be helpful in reducing inflammation and cardiovascular risk.

Calphostin C as a rapid and strong inducer of apoptosis in human coronary artery smooth muscle cells.

Vascular smooth muscle cells (VSMCs) play a major role in the development of atherosclerotic and restenotic lesions. The apoptotic process has been implicated in the development of this pathology. In this study, we characterized the induction of apoptosis by calphostin C (CC), a protein kinase C (PKC) inhibitor, in primary human coronary artery smooth muscle cells in the presence and absence of insulin-like growth factor-I (IGF-I). Additionally, we investigated the signal transduction pathways important for IGF-I mediated protection. Calphostin C induced apoptosis, as measured by terminal deoxy-UTP nick-end labeling (TUNEL), in a time- and dose-dependent manner, approaching 20% within 6 h of 50 nM calphostin C treatment. The amount of apoptosis increased to 44.58+/-8.08%, 47.54+/-1.66% and 78.1+/-11.9% after 8, 10 and 12 h of treatment, respectively (p<0.01 vs. control). IGF-I offered significant protection (p<0.05) at 8 and 10 h of treatment (60.6% and 52.5% protection, respectively). DNA ELISA confirmed the apoptotic effect of calphostin C and the protective effect of IGF-I. After 6 h of calphostin C treatment, DNA ELISA revealed 11.20+/-1.53 fold greater apoptosis as compared to baseline values. IGF-I treatment offered a level of protection of 46.6% as measured by DNA ELISA (p=0.06). Apoptosis was further qualitatively confirmed by time-lapse video microscopy and scanning electron microscopy. Interestingly, inhibitors of phosphatidylinositol-3-kinase (PI-3-K), p38 and extracellular regulated kinase (ERK) activation significantly (p<0.05 vs. calphostin C only treatment) increased apoptosis when used in conjunction with calphostin C. Inhibitors of phospatidylinositol-3-kinase and ERK activation reversed IGF-I protection. However, the p38 inhibitor SB203580 failed to reverse IGF-I protection. This study characterized an apoptotic system for human coronary artery smooth muscle cells offering a rapid and strong induction of programmed cell death (PCD) that remains responsive to the survival effects of IGF-I. Studies utilizing this system may prove useful in understanding the apoptotic response of VSMCs in the arterial wall.