Myocardial infarction with normal coronary angiogram. Possible mechanism of smoking risk in coronary artery disease.

McKenna, William J.; Chew, Christopher; Oakley, Celia M.

doi:10.1136/hrt.43.5.493

Cited by 80 publications

(20 citation statements)

References 13 publications

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“…It is also well known that cigarette smoking may predispose to myocardial infarction even with normal coronary arteries by means of coronary vasospasm [5][6][7]. Young heavy smokers with angiographically normal coronary arteries have an abnormal coronary vasoconstriction induced by acetylcholine [8], which means that NO is probably decreased locally.…”

Section: Dear Editormentioning

confidence: 97%

Effects of smoking on myocardial infarction at early ages

Yetkın

Tekin

Yağmur

et al. 2007

International Journal of Cardiology

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Section: Dear Editormentioning

confidence: 97%

Effects of smoking on myocardial infarction at early ages

Yetkın

Tekin

Yağmur

et al. 2007

International Journal of Cardiology

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“…Even in patients with angiographically normal coronary arteries, that is, no detectable atheromatous changes, cigarette smoking has been shown to be associated with vasospastic angina [47], which is most likely caused by enhanced local norepinephrine release, and an increased rate of myocardial infarction due to an occlusive coronary thrombus [33].…”

Section: Observations and Implications In Coronary Artery Diseasementioning

confidence: 99%

Nicotine and sympathetic neurotransmission

Haass

Kübler

1997

Cardiovasc Drug Ther

240

157

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Nicotine increases heart rate, myocardial contractility, and blood pressure. These nicotine-induced cardiovascular effects are mainly due to stimulation of sympathetic neurotransmission, as nicotine stimulates catecholamine release by an activation of nicotine acetylcholine receptors localized on peripheral postganglionic sympathetic nerve endings and the adrenal medulla. The nicotinic acetylcholine receptor is a ligand-gated cation channel with a pentameric structure and a central pore with a cation gate, which is essential for ion selectivity and permeability. Binding of nicotine to its extracellular binding site leads to a conformational change of the central pore, which results in the influx of sodium and calcium ions. The resulting depolarization of the sympathetic nerve ending stimulates calcium influx through voltage-dependent N-type calcium channels, which triggers the nicotine-evoked exocytotic catecholamine release. In the isolated perfused guinea-pig heart, cardiac energy depletion sensitizes cardiac sympathetic nerves to the norepinephrine-releasing effect of nicotine, as indicated by a leftward shift of the concentration-response curve, a potentiation of maximum transmitter release, and a delay of the tachyphylaxis of nicotine-evoked catecholamine release. This sensitization was also shown to occur in the human heart under in vitro conditions. Through the intracardiac release of norepinephrine, nicotine induces a beta-adrenoceptor-mediated increase in heart rate and contractility, and an alpha-adrenoceptor-mediated increase in coronary vasomotor tone. The resulting simultaneous increase in oxygen demand and coronary resistance has a detrimental effect on the oxygen balance of the heart, especially in patients with coronary artery disease. Sensitization of the ischemic heart to the norepinephrine-releasing effect of nicotine may be a trigger for acute cardiovascular events in humans, such as acute myocardial infarction and/or life-threatening ventricular tachyarrhythmias.

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“…This discrepancy is explained by the observation that many acute coronary events result from sudden occlusion of a previously unobstructed segment of the artery, while ST depression on exercise detects ischaemia from pre-existing stenosis [52]. The phenomenon of thrombosis in angiographically normal coronary arteries may be related to activation of a small, non-stenotic atherosclerotic plaque and appears more common among smokers [53, 54]. …”

Section: Recommended Baseline Work-upmentioning

confidence: 99%

Sudden Cardiac Death in the Young: A Strategy for Prevention by Targeted Evaluation

Sen‐Chowdhry

McKenna

2006

Cardiology

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The annual incidence of sudden cardiac death (SCD) in the general population is estimated as 1 in a 1,000. Since survival rates from out-of-hospital cardiac arrests are poor, primary prevention is key to reducing the burden of SCD in the community. Prominent causes of SCD include ischaemic heart disease, anomalous coronary arteries, and the primary myocardial diseases: hypertrophic cardiomyopathy, dilated cardiomyopathy, and ar rhythmogenic right ventricular cardiomyopathy (ARVC). In 4% of sudden deaths in the 16–64 age group, post-mortem examination fails to identify a cause, yielding a default diagnosis of sudden arrhythmic death syndrome (SADS). The inherited arrhythmia syndromes (long QT, short QT, and Brugada syndromes, and familial catecholaminergic polymorphic ventricular tachycardia) may be implicated in SADS, owing to their propensity for producing ventricular tachyarrhythmia in the structurally normal heart. Monogenic disorders therefore predominate as causes of SCD in the young. The advent of effective therapies for these diseases, particularly implantable cardioverter defibrillators, has prompted calls for universal screening to enable timely diagnosis of occult cardiac disease. Since prospective cardiac assessment of the general population is not feasible, the solution may be to target high-risk subgroups, namely, patients with cardiac symptoms, relatives of SCD victims, and competitive athletes. The recommended preliminary work-up includes a 12-lead ECG, signal-averaged ECG, transthoracic echocardiogram, exercise test, and ambulatory ECG monitoring. Cardiovascular magnetic resonance is a useful adjunct in patients with suspected ARVC or anomalous coronary arteries. Provocative challenge with a sodium challenge blocker may be of value in unmasking the Brugada syndrome. Identification of disease-causing mutations in affected individuals facilitates cascade screening of families.

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Myocardial infarction with normal coronary angiogram. Possible mechanism of smoking risk in coronary artery disease.

Cited by 80 publications

References 13 publications

Effects of smoking on myocardial infarction at early ages

Effects of smoking on myocardial infarction at early ages

Nicotine and sympathetic neurotransmission

Sudden Cardiac Death in the Young: A Strategy for Prevention by Targeted Evaluation

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