Effect of Cigarette Smoking and Breathing Carbon Monoxide on Cardiovascular Hemodynamics in Anginal Patients

Abstract

Smoking high-nicotine cigarettes caused a significant increase in systolic and diastolic arterial pressure, heart rate, left ventricular end-diastolic pressure, and coronary sinus, arterial, and venous CO levels, no significant change in left ventricular dp/dt, aortic systolic ejection period, and cardiac index, and a significant decrease in stroke index and coronary sinus, arterial, and venous P02 levels in eight anginal patients with documented coronary disease. One week later, these patients inhaled 150 ppm of carbon monoxide until their increase in coronary sinus CO was similar to that produced after smoking their third cigarette. Inhaling carbon monoxide caused a significant increase in left ventricular end-diastolic pressure and coronary sinus, arterial, and venous CO levels, no significant change in systolic and diastolic arterial pressure, heart rate, and systolic ejection period, and a significant decrease in left ventricular dp/dt, stroke index, cardiac index, and coronary sinus, arterial, and venous PO2 levels. Nicotine caused the increased systolic and diastolic arterial pressure and heart rate after smoking. Carbon monoxide caused the negative inotropic effect which increased the left ventricular end-diastolic pressure and decreased the stroke index after smoking.

Influence of Moderately Elevated Levels of Carboxyhemoglobin on the Course of Acute Ischemic Heart Disease

“…The main effects of nicotine on the cir culatory system are sympathomimetic: a rise of blood pressure, pulse rate and heart minute volume, a positive inotropic effect and peripheral vasoconstriction, resulting in an increase in myocardial oxygen de mand [21][22][23]. CO impairs myocardial performance and oxygen delivery.…”

Impact of Smoking on the Atrial Substrate Characteristics in Patients with Atrial Fibrillation

“…10 In the presence of coronary-artery stenosis, the coronary flow can not increase and ischemia may develop, with resultant angina pectoris or myocardial dysfunction. 11,12 Recently, Barua RS, et al demonstrated that smoking could cause dysfunction of the nitric oxide biosynthesis in endothelium cells by oxdative stress 9 and that mechanism may further impair the endothelium-dependent coronary artery dilatation capability and reduce the myocardial oxygen supply.…”

“…[10][11][12][13][14] Cigarette consumption is directly related to increased rates of sudden cardiac death (SCD), mainly through its direct toxic effects. Recently, the impact of the smoking status on SCD was studied in patients with established coronary artery 15 In that study, current cigarette smoking was a powerful independent predictor of the SCD risk and those that quit smoking experienced a significant reduction in the SCD risk.…”

Carbon Monoxide, Nicotine and the ‘Safer’ Cigarette

“…While nicotine increases the cardiac work load, carbon monoxide decreases the deliv ery of oxygen to the myocardium [12,36,37]. The development of electrocardiograph ic changes indicating myocardial ischaemia is thus well recognized in severe carbon monoxide intoxication.…”