Abstract
Passive and active chronic cigarette smoking (CS) remains an international epidemic and a key risk factor for cardiovascular disease (CVD) development. CS-induced cardiac damage is divided into two major and interchangeable mechanisms: (1) direct adverse effects on the myocardium causing smoking cardiomyopathy and (2) indirect effects on the myocardium by fueling comorbidities such as atherosclerotic syndromes and hypertension that eventually damage and remodel the heart. To date, our understanding of cardiac remodeling following acute and chronic smoking exposure is not well elucidated. This manuscript presents for the first time the RIMD (oxidative stress (R), inflammation (I), metabolic impairment (M), and cell death (D)) detrimental cycle concept as a major player in CS-induced CVD risks and direct cardiac injury. Breakthroughs and latest findings in the field with respect to structural, functional, cellular, and molecular cardiac remodeling following chronic smoking exposure are summarized. This review also touches the genetics/epigenetics of smoking as well as the smoker's paradox and highlights the most currently prominent pharmacological venues to mitigate CS-induced adverse cardiac remodeling.
Highlights
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide
This review highlights the effect of chronic tobacco smoking (CS) on structural, functional, and molecular cardiac remodeling based on most recent breakthroughs and latest publications
This study revealed impaired mitochondrial respiration through enhanced lactate dehydrogenase activity and decreased citrate synthase activity, and an Structural/functional changes (i) Normal function (ii) Normal structure
Summary
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide. The World Health Organization (WHO) estimates a total of 17.5 million annual CVD deaths (31% of total death) mostly due to myocardial infarction (MI) and strokes (http://www.who .int/cardiovascular_diseases/en/). WHO estimates a total of 5 million deaths yearly due directly to tobacco smoke and more than 600,000 deaths due to second-hand smoke. People who are exposed to second-hand smoke are at a 25–30% risk of developing heart disease and 20–30% risk of stroke [1]. Multiple studies show that oxidative compounds are primarily responsible of smoking-mediated myocardial injury [3, 5,6,7,8,9], the exact mechanisms of numerous potentially harmful smoke compounds remain poorly understood and require further investigation. Promising pharmacological interventions that protect the heart from the cigarette smoking epidemic are summarized in this manuscript
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