Cigarette smoking is a leading preventable risk factor for the development and progression of cardiovascular diseases (CVDs). Epidemiologic studies conclusively prove that both active smoking and secondhand smoke contribute significantly to morbidity and mortality related to CVD. Cigarette smoke is a mixture of several toxic chemicals, of which nicotine, carbon monoxide, and oxidant chemicals are most commonly implicated in the pathogenesis of cardiovascular disease. Tobacco causes endothelial dysfunction, inflammation, insulin resistance, alteration of lipid profile, hemodynamic alterations, and a hypercoagulable state. All of these act synergistically as pathobiologic mechanisms of atherothrombosis in tobacco users.

This study, using validation with CTA, showed that conventional ECG criteria and fluoroscopy are inaccurate in differentiating septal from anterior RVOT pacing. The fluoroscopic lateral view, as corroborated by CTA, is more reliable than the LAO view in predicting septal lead placement.

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Inflammation may be an important contributing factor to the progression of Eisenmenger syndrome (ES). Markers of systemic inflammation in ES have not been systematically studied. Inflammatory markers including high-sensitivity C-reactive protein (hs-CRP), interleukin-2 (IL-2), IL-6, and interferon-γ (IFN-γ) were measured in 42 consecutive ES patients (mean age, 24.3 ± 10.6 years) compared with their levels in 22 healthy control subjects. The patients were followed up for a mean duration of 16.3 ± 13.7 months. The levels of inflammatory markers were correlated with clinical and hemodynamic variables at baseline and the outcomes of death, hospitalization, and worsening World Health Organization (WHO) functional class at follow-up evaluation. Compared with the control subjects, ES patients showed a significant elevation in hs-CRP (2.99 ± 3.5 vs 1.1 ± 0.9 mg/dl; p = 0.002) and IFN-γ (41.3 ± 43.6 vs 10.4 ± 6.9 pg/ml; p < 0.001) levels. The levels of IL-2 and IL-6 also were elevated but did not differ significantly from those in the control subjects. The patients with hs-CRP levels higher than 3 mg/dl were significantly older (28.9 ± 10.6 vs 21.5 ± 9.8 years) and had a significantly shorter 6-min walk distance (421.5 ± 133.2 vs 493.3 ± 74.8 m). The levels of inflammatory markers did not correlate with baseline parameters or clinical outcomes. To conclude, the levels of hs-CRP and IFN-γ are significantly elevated in ES. Elevated hs-CRP in ES was associated with older age and shorter 6-min walk distance, but the levels of inflammatory markers were not predictive of clinical events.

A 72-year-old gentleman was brought to the emergency department, after sustaining an allegedly accidental airgun-shot injury to the right side of his neck. A chest radiograph and plain CT chest revealed the bullet lodged deeply in the soft tissues of the right side of the neck. He was taken up for an emergency neck exploration for foreign

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Cardiogenic shock continues to be the most common cause of death in patients with acute myocardial infarction (MI), occurring in 5-10% of ST-elevation MIs (STEMI) and 2-3% of non-ST-elevation acute coronary syndromes (ACS). A complex, degenerating clinical spiral of multiorgan dysfunction, cardiogenic shock begins when the heart is no longer able to provide sufficient resting pressure and flow. 1 Without effective intervention, progression of cardiogenic shock is rapid and fatal. 2 Over the past decade, although the rates of cardiogenic shock present on hospital admission have remained constant, the overall incidence has decreased. This may be attributed to the increased global frequency of revascularisation for ACS. The AMIS Plus Registry 3 of 23,696 patients with ACS provides good proof for this. The overall incidence of cardiogenic shock from 1997 to 2006 fell from 12.9% to 5.5% (P < 0.001), while the use of primary percutaneous coronary intervention (PPCI) during the same period in patients with cardiogenic shock increased from 7.6% to 65.9% (P = 0.01) and was associated with a lower hospital mortality (odds ratio 0.47, 95% confidence interval 0.30-0.73, P = 0.001). The rates of cardiogenic shock on admission remained constant (28.5% of all cases; 2.3% of those with ACS). However, the incidence of shock developing in patients with MI after admission fell from 10.6% to 2.7% (P < 0.001) and in-hospital shock mortality fell from 62.8% to 47.7% (P = 0.010).Despite advances and innovations in the management of cardiogenic shock, the rates of mortality, although improved to an extent in the recent decades, remain strikingly high. In the 1970s, the outlook of survival for patients with cardiogenic shock was dismal, with rates of in-hospital mortality exceeding 80%. For the past two decades, rates of survival have improved; however, approximately 50% of patients with cardiogenic shock still do not survive to hospital discharge. In this issue of the journal, Mullasari et al. studied 41 patients who underwent PPCI or rescue PCI for acute MI complicated by cardiogenic shock. 4 The 30-day mortality rate of this group of patients was 56.1%. Such substantial figures are shared by other studies too. In the Arbeitsgemeinschaft Leitende Kardiologische Krankenhausarzte registry with 1333 patients with cardiogenic shock, total in-hospital mortality was 46.1%. 5 Similarly, the overall survival in the PCI arm of the (Should we emergently revascularise occluded coronaries for cardiogenic shock?) SHOCK trial was 54% at 30 days and 50% at 1 year. 6 Although, early shock-related mortality remains significant with improving medical and interventional therapy, the outlook for survivors of ACS may be increasingly optimistic. 7,8 In the SHOCK trial, the mortality rates in the two groups of revascularisation and medical treatment were not statistically significant at 30 days (46.7% vs 56%, respectively, P = 0.11), but by 6 months there was difference in benefit, and significantly increased survival rates were observed in patients treated...

Background Resistance to antiplatelet drugs is a wellknown entity. However, data for aspirin and clopidogrel resistance, and its clinical significance, in Indian patients are meagre. Aims and objectives We sought to determine the prevalence of resistance to aspirin and clopidogrel in Indian patients with stable coronary heart disease (CHD), using the cone and plate(let) analyser (CPA) technology. Setting and design A single centre prospective study in a cohort of patients with stable CHD on chronic aspirin and clopidogrel therapy attending the cardiology outpatient clinic of a tertiary care hospital in Southern India. Methods Platelet function was measured using the Impact-R device (DiaMed, Cressier, Switzerland). Resistance to aspirin and clopidogrel was measured in a cohort of 100 patients with stable documented CHD. Relation of antiplatelet resistance to various clinical comorbidities was also assessed. Results Of the 100 patients, 85% were men, and 15% were above 65 years of age. 47% patients had diabetes, 29% of patients were hypertensive and 16% were smokers. Using the CPA, 12 patients (12%) were found to be resistant to aspirin and 19 patients (19%) were clopidogrel resistant. In addition, 10 patients (10%) were resistant to both aspirin and clopidogrel. There was no significant correlation between the presence of antiplatelet resistance and several baseline clinical variables, including age, sex, diabetes, hypertension and smoking. Conclusions Resistance to aspirin and clopidogrel and dual antiplatelet resistance are prevalent in Indian patients, comparable with the prevalence worldwide. The CPA is a feasible assay to determine antiplatelet resistance.