Association of polymorphisms at LDLR locus with coronary artery disease independently from lipid profile

Coronary artery disease [CAD] is the leading cause of mortality in many parts of the world. Genome-wide association studies [GWAS] have identified several genetic variants associated with CAD in Low-density lipoprotein receptor [LDLR] locus. This study was evaluated the possible association of genetic markers at LDLR locus with CAD irrespective to lipid profile and as well as the association of these SNPs with severity of CAD in Iranian population. Sequencing of 2 exons in LDLR gene [Exon 2, 12] and part of intron 30 of SMARCA4 gene include rs1122608, was performed in 170 Iranian patients angiographically confirmed CAD and 104 healthy controls by direct sequencing. Sullivan's scoring system was used for determining the severity of CAD in cases. Our results showed that homozygote genotypes of rs1122608 [P<0.0001], rs4300767 [P<0.005] and rs10417578 [p<0.007] SNPs have strong protective effects on the CAD. In addition, we found that rs1122608 [GT or TT] was at higher risk of three vessel involvement compared to single vessels affecting [P=0.01]

Difficult management of coronary artery disease in a patient with thrombotic thrombocytopenic purpura

Thrombotic thrombocytopenic purpura [TTP] is a rare syndrome affecting multiple organs. There is no sufficient evidence regarding the clinical cardiac manifestations of TTP. Nonetheless, pathologic cardiac involvement is quite frequent in acute TTP, which is predominantly manifested as myocardial necrosis due to coronary arteriolar microthrombosis. The present case report describes a 43-year-old man with long-standing remitted TTP, who suffered from a sequence of refractory thrombotic epicardial coronary events. Aggressive medical and interventional therapies, including long-term dual antiplatelets and coronary angioplasty, were finally successful in remitting the thrombotic events. During his two-year follow up, he has been asymptomatic

Risk factors of reperfusion failure following primary angioplasty for ST-segment elevation myocardial infarction [STEMI]

Although percutaneous coronary intervention [PCI] improves outcomes compared to thrombolysis, a substantial number of ST-elevation myocardial infarction [STEMI] patients do not achieve optimal myocardial reperfusion. This study was designed to evaluate factors related to suboptimal myocardial reperfusion after primary PCI in patients with STEMI. Totally, 155 patients [124 men; mean age = 56.6 +/- 11.03 years, range = 31- 85 years] with STEMI undergoing primary PCI were retrospectively studied. Additionally, the relationships between the occurrence of reperfusion failure and variables such as age, sex, cardiac risk factors, family history, Body Mass Index, time of symptom onset, ejection fraction, previous PCI, coronary artery bypass graft surgery or previous myocardial infarction, and angiographic data were analyzed. Procedural success was 97.1% and complete ST resolution occurred in 43.2%. Age; cardiac risk factors; family history; body mass index; previous MI, coronary artery bypass graft surgery, or PCI; and use of thrombectomy device and GP2b/3a inhibitor were not the determining factors [p value > 0.05]. According to our multivariate analysis, time of symptom onset [OR [95% CI]: 045 [0.2 to 0.98]; p value = 0.044] and ejection fraction [OR [95% CI]:0.37 [0.26 to .091]; p value = 0.050] had reverse and male gender had direct significant associations with failed reperfusion [OR [95% CI]: 0.34 [0.11 to 1.08]; p value = 0.068]. More degrees of ST resolution occurred when the right coronary artery was the culprit vessel [p value = 0.001]. The presence of more than three cardiac risk factors was associated with failed reperfusion [p value = 0.050]. Considering the initial risk profile of patients with acute STEMI, including time of symptom onset and ejection fraction, as well as the accumulation of cardiac risk factors in a given patient, we could predict failed myocardial reperfusion to design a more aggressive therapeutic strategy

Intracoronary adenosine to prevent myonecrosis in patients with stable angina undergoing percutaneous interventions: a double-blinded randomized controlled trial

Significant elevation of cardiac biomarkers after percutaneous coronary intervention [PCI] is associated with increased mortality. However, clinical importance of lesser degrees of cardiac enzyme elevation has not been well understood. Multiple factors might have an etiologic role, and the incidence of myonecrosis has not changed dramatically despite pharmacological and technological advances in PCI. The aim of this study was to evaluate the role of intracoronary [1C] Adenosine in preventing the elevation of cardiac enzymes as a marker of myonecrosis after PCI in patients with chronic stable angina. Two hundred sixty patients with chronic stable angina who were candidates for PCI were randomly assigned to double-blinded pretreatment with 1C Adenosine or placebo before crossing of the guide wire. The patients were observed during the hospital course, and blood samples were obtained in standard intervals after the intervention for cardiac biomarkers. The primary end point of this study was post-PCI myonecrosis, and secondary end point was safety of 1C Adenosine administration in the setting of PCI in patients with chronic stable angina. Of the 260 patients, who were initially randomized, finally 83 patients were analyzed in the placebo and 96 in the Adenosine arms. The study patients were comparable in clinical and angio graphic characteristics. The mean of the patients age was 57.3 years [range = 35 to 79 years], and 77.5% were male. There were no differences in the mean serum cardiac biomarkers between the study groups [mean creatine kinase-MB [CK.MB] level of 29.5 +/- 14.5 IU/L in the placebo group and 31.5 +/- 18.5 IU/L in the control group; p value = 0.41; mean cardiac troponin I [cTnI] level of 0. 097 _0.178 microg/L in the placebo group and 0.167 +/- 0.5 microg/L in the control group; p value = 0.24]. Despite promising results in primary PCI, our study showed that a strategy of 1C Adenosine pretreatment is not beneficial in reducing post-PCI myonecrosis in patients with chronic stable angina and should not be routinely used

Percutaneous device closure for secundum-type atrial septal defect: short and intermediate-term results

Device closure of an isolated secundum type atrial septal defect [ASD] has been used as an alternative method for open surgical closure with comparable success and lower morbidity. In this study we evaluated the procedural success and mid-term follow-up results of percutaneous closure of secundum ASD with an Amplatzer TM Septal Occluder [ASO] device or a Figula ASD occluder device. From June 2001 to January 2009, 74 consecutive patients were scheduled for percutaneous device closure in two centers in Tehran, Iran. All patients had a stretched defect diameter of 30mm or less. After using a sizing balloon to measure the stop-flow diameter, device implantation was performed under the guidance of a trans-esophageal echocardiography [TEE].The size was generally 1 - 2 mm larger than the stretched diameter. Patients were followed for an average of 11 +/- 4 months. The median stretched diameter of the defect was 20.7 +/- 4.8 mm [range: 8 - 30 mm].A total of 73 devices were used in this study. Device closure was successful in 72 [97.2%] out of 74 patients. Repositioning of the device was required in one patient. Major complications [including significant residual shunt and device embolization] occurred in 3 [4%] patients. There was no procedure-related mortality in our patients. Mild-to-moderate residual shunt was detectable in 10 [13.7%] patients immediately following the procedure and in 5 [6.7%] patients 24 hours after the procedure. None had residual flow across the device at the end of the follow-up period. Device closure of ASD has a safety profile comparable to open surgical repair and can effectively close the defect with excellent procedural and mid-term results

Carbapenem resistance in gram-negative bacilli isolates in an Iranian 1000-bed tertiary hospital

Carbapenems are beta-lactamase antibiotics, presently considered as most potent agents for treatment of infections caused by Gram-negative bacilli. The aim of this study was to determine resistance of Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella pneumonniae as prevalent nosocomial agents to commonly used antibiotics including carbapenems such as imipenem and meropenem. A total of 202 gram-negative bacilli including K. pneumoniae, P aeruginosa and A. baumannii isolated from hospitalized patients in Milad hospital of Tehran were subject for susceptibility testing. Susceptibility testing was performed by disk diffusion and MIC methods as recommended by Clinical Laboratory Standards Institute [CLSI]. All isolates of K. pneumonia were susceptible to imipenem and meropenem. Resistance in non-fermenting gram-negative bacilli [NFGB] was prevalent. P. aeruginosa isolates exhibited 7.5% and 40.2% resistance to imipenem and meropenem respectively. The majority isolates of Acinetobacter baumannii were multi-drug resistant and resistance of this organism to imipenem and meropenem was 27.7% and 38.5% respectively. Our study revealed that in spite of resistance of K. pneumoniae to commonly used antibiotics, all isolates were susceptible to imipenem and meropeem. More than 80% isolates of A. bammanni were resistant to commonly used antibiotics. About 40.2% isolates of P. aeruginosa and [38.5%] isolates of A. baumannii were resistant to meropenem respectively