Background:Chronic obstructive pulmonary disease (COPD) is a major cause of mortality and morbidity. It is the fourth leading cause of death worldwide. Acute exacerbations of COPD are common and are associated with worsening lung function and mortality.Objectives:To evaluate the prevalence of elevation of cTnI in patients admitted with acute exacerbation of COPD and to study its association with the need for ventilator support, duration of hospital stay, and in-hospital mortality.Methods:In a prospective design, 50 patients admitted to our hospital with acute exacerbation of COPD were included. cTnI was assayed in a blood sample obtained at admission and 24 h later. Levels above 0.017 µg/L were taken as positive. The following data were also recorded–demographic data, pattern of tobacco use, clinical symptoms and signs, comorbidities, Glasgow Coma Scale, arterial blood gas, electrocardiogram/two-dimensional echocardiography, chest X-ray, and peak expiratory flow rate.Results:Among the 50 patients, 4 were females, and 46 were males. cTnI was positive in 32% of patients with a mean value of 0.272. Patients with cTnI positive were taken as Group I and those with negative were included in Group II. Prevalence of comorbidities was higher in cTnI positive group, so was the duration of COPD. cTnI elevation correlated significantly with the need for ICU admission and ventilator support. No significant difference was found in the duration of ventilator support, hospital stay, and in-hospital mortality.Conclusion:cTnI is elevated in a significant subset of patients with acute exacerbation of COPD. Duration of their illness was longer, higher incidence of ischemic heart disease was also found in these patients. Patients with cTnI elevation are more likely to require ICU care and ventilator support. However, it did not predict in-hospital mortality. Thus, it can be used as a marker to identify high-risk patients during acute exacerbation of COPD.
Familial hypercholesterolemia is a rare, monogenic, co-dominant, life-threatening disorder resulting from loss of function mutations in the genes responsible for synthesis of low-density lipoprotein receptors or apo-B genes or gain of function mutations in PCSK9 genes in the liver which affects 0.2% of the population. It is characterized by severe lifelong elevation of LDL cholesterol and by development of xanthelasma, xanthomas, premature coronary artery disease and peripheral artery occlusive disease. Most patients develop PCAD and aortic stenosis before the age of 20 years and die before 30 years of age. The diagnosis of FH is usually based on clinical presentation and commonly used criteria are the Dutch lipid clinic network criteria, Simon Broome criteria or the WHO criteria. We encountered four cases of familial hypercholesterolemia over last 10 years. All the four patients presented with effort angina and all were found to have obstructive coronary artery disease oncoronary angiogram and two of them had severe supravalvular aortic stenosis. All four patients were on dietary modifications, high intensity statin and cholesterol absorption inhibitor. Two patients underwent coronary artery bypass grafting with aortoplasty, one patient underwent coronary artery bypass grafting and one patient underwent percutaneous transluminal coronary angioplasty. Familial hypercholesterolemia leads to development of life-threatening manifestations early in the second and third decades of life. Early diagnosis, aggressive treatment and control of risk factors and cascade screening are important in management and will help to reduce the morbidity and mortality associated with this disease.
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