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ObjectiveTo investigate the effect of passive smoking, active smoking and smoking cessation on inflammation, lipid profile and the risk of myocardial infarction (MI).MethodsA total of 423 cases with a first MI and 465 population controls from the Maltese Acute Myocardial Infarction (MAMI) Study were analysed. Data were collected through an interviewer-led questionnaire, and morning fasting blood samples were obtained. ORs adjusted for the conventional risk factors of MI (aORs) were calculated as an estimate of the relative risk of MI. The influence of smoking on biochemical parameters was determined among controls.ResultsCurrent smokers had a 2.7-fold (95% CI 1.7 to 4.2) and ex-smokers a 1.6-fold (95% CI 1.0 to 2.4) increased risk of MI. Risk increased with increasing pack-years and was accompanied by an increase in high-sensitivity C reactive protein levels and an abnormal lipid profile. Smoking cessation was associated with lower triglyceride levels. Exposure to passive smoking increased the risk of MI (aOR 3.2 (95% CI 1.7 to 6.3)), with the OR being higher for individuals exposed to passive smoking in a home rather than in a public setting (aOR 2.0 (95% CI 0.7 to 5.6) vs aOR 1.2 (95% CI 0.7 to 2.0)). Passive smoke exposure was associated with higher levels of total cholesterol, triglycerides and total cholesterol:high-density lipoprotein cholesterol ratio compared with individuals not exposed to passive smoking.ConclusionsBoth active and passive smoking are strong risk factors for MI. This risk increased with increasing pack-years and decreased with smoking cessation. Such effects may be partly mediated through the influence of smoking on inflammation and lipid metabolism.

Inability to cross the lesion with a guidewire is the most common reason for failure in percutaneous revascularization (PCI) of chronic total occlusions (CTOs). An ostial or stumpless CTO is an acknowledged challenge for CTO recanalization due to difficulty in successful wiring. IVUS imaging provides the opportunity to visualize the occluded vessel and to aid guidewire advancement. We review the value of this technique in a single-centre experience of CTO PCI. This series involves 22 patients who underwent CTO-PCI using IVUS guidance for stumpless CTO wiring at our institution. CTO operators with extensive IVUS experience in non-CTO cases carried out all procedures. Procedural and outcome data was prospectively entered into the institutional database and a retrospective analysis of clinical, angiographic and technical data performed. 17 (77%) of the 22 procedures were successful. The mean age was 59.8 ± 11.5 years, and 90.9% were male. The most commonly attempted lesions were located in the left anterior descending 36.4% (Soon et al. in J Intervent Cardiol 20(5):359-366, 2007) and Circumflex artery (LCx) 31.8% (Mollet et al. in Am J Cardiol 95(2):240-243, 2005). Mean JCTO score was 3.09 ± 0.75 (3.06 ± 0.68, 3.17 ± 0.98 in the successful and failed groups respectively p = 0.35). The mean contrast volume was 378.7 ml ± 114.7 (389.9 ml ± 130.5, 349.2 ml ± 52.2 p = 0.3 in the successful and failed groups respectively). There was no death, coronary artery bypass grafting or myocardial infarction requiring intervention in this series. When the success rates were analyzed taking into account the date of adoption of this technique, the learning curve had no significant impact on CTO-PCI success. This series describes a good success rate in IVUS guided stumpless wiring of CTOs in consecutive patients with this complex anatomical scenario.

Aim To determine the risk of myocardial infarction (MI) associated with pattern, frequency, and intensity of alcohol consumption, type of alcoholic beverage, and the combined effect of alcohol and smoking on risk of MI, inflammation, and lipid profile. Method A total of 423 cases with a first MI and 465 controls from the Maltese Acute Myocardial Infarction (MAMI) Study were analysed. Data was collected through an extensive interviewer-led questionnaire, along with measurements of various blood parameters. Medians and the Mann-Whitney test were used to assess effect of different drinking patterns, frequency, intensity, and smoking and drinking combinations on hs-CRP and lipid profile. Odds ratios, adjusted for the conventional risk factors of MI (AdjORs), were calculated as an estimate of the relative risk of MI. Results Regular alcohol consumption protected against MI [AdjOR 0.6 (95% CI 0.4-0.9)] while daily binge drinking increased risk [AdjOR 5.0 (95% CI 1.6-15.0)] relative to regular drinkers who did not binge drink. Whereas moderate weekly consumption of wine protected against MI, high weekly consumption of beer conveyed a deleterious effect. Alcohol consumption decreased risk of MI independent of smoking status. Frequent alcohol consumption was associated with higher HDL-, non-HDL-, total cholesterol and triglycerides, and lower hs-CRP. Total and HDL-cholesterol increased and BMI decreased with increasing quantity of weekly alcohol consumption relative to the non-regular drinkers. The effect of smoking on lipid profile and hs-CRP was less pronounced in current drinkers than in those who were non-regular drinkers. Conclusion The protective effect of alcohol consumption was dependent on the pattern, frequency, type, and intensity of alcohol consumed. Alcohol modified the effects of smoking on the lipid profile. Regular drinking attenuated the effect of smoking on hs-CRP and lipid profile.