Acute effects of cigarette smoking on the cardiac diastolic functions

Smoking is an independent risk factor for coronary heart diseases and it increases all causes of cardiovascular morbidity and mortality. To assess the acute effect of cigarette smoking on ventricular diastolic functions [LV and RV] in healthy, young, and slim smokers. Thirty volunteers who had recently commenced smoking [less than one year] and who smoked 1-2 cigarettes per day, underwent ECG, 2D and M-mode echocardiography, standard Doppler echocardiography, pulsed TDI [tissue Doppler imaging] on septal and lateral side of mitral annulus and lateral tricuspid annulus. Vp values were measured. The investigator asked them to hold smoking for at least two days after which echocardiographic examination was conducted before smoking one cigarette and the second examination conducted immediately after smoking one cigarette containing at least 0.4 mg of nicotine. Doppler findings over the mitral valve showed the E wave was significantly reduced from 82.7 +/- 10.4 to 74.6 +/- 10.4 after smoking; the A wave increased; the E/A ratio was reduced from 1.5 +/- 0.3 to 1.2 +/- 0.2; the E' septal significantly decreased [15.3 +/- 2.4 vs. 11.2 +/- 1.1] after smoking, and the E/E' ratio increased from 5.5 +/- 1.1 to 6.7 +/- 1.1. Doppler findings over the tricuspid valve showed the E wave was reduced from 60.6 +/- 9.7 to 52.7 +/- 9.6; the A wave increased from 42.2 +/- 6.5 to 50.1 +/- 6.6; and the E/A ratio decreased [1.45 +/- 0.25 vs. 1.06 +/- 0.19]. The E' significantly decreased from 14.1 +/- 1.8 to 10.9 +/- 2.4, while the A' increased [10.2 +/- 2.4 vs. 12.7 +/- 3.6] after smoking; and the IVRT of the RV was significantly prolonged from 62.9 +/- 7.5 to 68.7 +/- 7.9 after smoking. The Vp was markedly reduced from 67.8 +/- 8 to 55.2 +/- 3.5 after smoking. These findings reflected on the LV filling pressure [LVFvp] which increased from 9.8 +/- 1.4 to 10.5 +/- 1.3 after smoking. All changes were statistically significant at P < 0.001. Our study reveals that cigarette smoking can result in significant acute alteration in the diastolic functions of both ventricles

Acute myocardial infarction associated with acute gouty arthritis

The association of hyperuricemia with increased risk of atherosclerosis has been reported in previous studies but the link of acute gouty arthritis, hyperuricemia and acute myocardial infarction [MI] is not seen frequently. Here we report a 33 year old male who presented with hyperuricemia, acute gouty arthritis and acute myocardial infarction. Hyperuricemia contributed not only to accelerated atherosclerosis but might be blamed for promoting environment for acute myocardial infarction

Metabolic syndrome and cardiovascular risk

The constellation of dyslipidemia [hypertriglyceridemia and low levels of high-density lipoprotein cholesterol], elevated blood pressure, impaired glucose tolerance, and central obesity is now classified as metabolic syndrome, also called syndrome X. In the past few years, several expert groups have attempted to set forth simple diagnostic criteria for use in clinical practice to identify patients who manifest the multiple components of the metabolic syndrome. These criteria have varied somewhat in specific elements, but in general, they include a combination of multiple and metabolic risk factors. The most widely recognized of the metabolic risk factors are atherogenic dyslipidemia, elevated blood pressure, and elevated plasma glucose. Individuals with these characteristics, commonly manifest a prothrombotic state as well as and a proinflammatory state. Atherogenic dyslipidemia consists of an aggregation of lipoprotein abnormalities including elevated serum triglyceride and apolipoprotein B [apoB], increased small LDL particles, and a reduced level of HDL cholesterol [HDL-C]. The metabolic syndrome is often referred to as if it were a discrete entity with a single cause. Available data suggest that it truly is a syndrome, ie, a grouping of atherosclerotic cardiovascular disease [ASCVD] risk factors, that probably has more than one cause. Regardless of cause, the syndrome identifies individuals at an elevated risk for ASCVD. The magnitude of the increased risk can vary according to the components of the syndrome present as well as the other, non-metabolic syndrome risk factors in a particular person