Association Between High-Sensitivity Cardiac Troponin Levels and Myocardial Ischemia During Mental Stress and Conventional Stress

Hammadah, Muhammad; Mheid, Ibhar Al; Wilmot, Kobina; Ramadan, Ronnie; Alkhoder, Ayman; Obideen, Malik; Abdelhadi, Naser; Fang, Shuyang; Ibeanu, Ijeoma; Pimple, Pratik; Kelli, Heval Mohamed; Shah, Amit; Pearce, Bradley D.; Sun, Yan V.; Garcia, Ernest; Kutner, Michael; Long, Qi; Ward, Laura; Bremner, J. Douglas; Esteves, Fábio; Raggi, Paolo; Sheps, David S.; Vaccarino, Viola; Quyyumi, Arshed A.

doi:10.1016/j.jcmg.2016.11.021

Cited by 31 publications

(18 citation statements)

References 35 publications

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“…Taken together, our study shows, for the first time that the health of the coronary microvascular endothelium, at least partly determines coronary vasodilation during psychological stress, and the latter is reflected in the peripheral microvascular vasomotor responses during MS. These findings illustrate potential mechanisms in the pathogenesis of MSIMI that occurs frequently in patients with CAD and is associated with poor outcomes . We have previously shown that lower digital microvascular reactivity is associated with MSIMI .…”

Section: Discussionsupporting

confidence: 59%

Coronary and Peripheral Vasomotor Responses to Mental Stress

Hammadah

Kim

Mheid

et al. 2018

JAHA

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BackgroundCoronary microvascular dysfunction may contribute to myocardial ischemia during mental stress (MS). However, the role of coronary epicardial and microvascular function in regulating coronary blood flow (CBF) responses during MS remains understudied. We hypothesized that coronary vasomotion during MS is dependent on the coronary microvascular endothelial function and will be reflected in the peripheral microvascular circulation.Methods and ResultsIn 38 patients aged 59±8 years undergoing coronary angiography, endothelium‐dependent and endothelium‐independent coronary epicardial and microvascular responses were measured using intracoronary acetylcholine and nitroprusside, respectively, and after MS induced by mental arithmetic testing. Peripheral microvascular tone during MS was measured using peripheral arterial tonometry (Itamar Inc, Caesarea, Israel) as the ratio of digital pulse wave amplitude compared to rest (peripheral arterial tonometry ratio). MS increased the rate‐pressure product by 22% (±23%) and constricted epicardial coronary arteries by −5.9% (−10.5%, −2.6%) (median [interquartile range]), P=0.001, without changing CBF. Acetylcholine increased CBF by 38.5% (8.1%, 91.3%), P=0.001, without epicardial coronary diameter change (0.1% [−10.9%, 8.2%], P=not significant). The MS‐induced CBF response correlated with endothelium‐dependent CBF changes with acetylcholine (r=0.38, P=0.03) but not with the response to nitroprusside. The peripheral arterial tonometry ratio also correlated with the demand‐adjusted change in CBF during MS (r=−0.60, P=0.004), indicating similarity between the microcirculatory responses to MS in the coronary and peripheral microcirculation.ConclusionsThe coronary microvascular response to MS is determined by endothelium‐dependent, but not endothelium‐independent, coronary microvascular function. Moreover, the coronary microvascular responses to MS are reflected in the peripheral microvascular circulation.

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Section: Discussionsupporting

confidence: 59%

Coronary and Peripheral Vasomotor Responses to Mental Stress

Hammadah

Kim

Mheid

et al. 2018

JAHA

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“…High‐sensitivity troponin I (hsTnI) was measured using the Abbott ARCHITECT analyzer (Abbott Laboratories, North Chicago, IL), which has a limit of detection of 1.2 pg/mL and an interassay coefficient of variation of <10% at 4.7 pg/mL. The upper reference limit (99th centile) ranges between 24 and 30 pg/mL in healthy populations, with a sex‐specific upper reference range of 36 pg/mL for men and 15 pg/mL for women . Samples were centrifuged twice before analysis and according to manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

High‐Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long‐Term Outcomes

Tahhan

Sandesara

Hayek

et al. 2018

JAHA

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BackgroundThe associations between high‐sensitivity troponin I (hsTnI) levels and coronary artery disease (CAD) severity and progression remain unclear. We investigated whether there is an association between hsTnI and angiographic severity and progression of CAD and whether the predictive value of hsTnI level for incident cardiovascular outcomes is independent of CAD severity.Methods and ResultsIn 3087 patients (aged 63±12 years, 64% men) undergoing cardiac catheterization without evidence of acute myocardial infarction, the severity of CAD was calculated by the number of major coronary arteries with ≥50% stenosis and the Gensini score. CAD progression was assessed in a subset of 717 patients who had undergone ≥2 coronary angiograms >3 months before enrollment. Patients were followed up for incident all‐cause mortality and incident cardiovascular events. Of the total population, 11% had normal angiograms, 23% had nonobstructive CAD, 20% had 1‐vessel CAD, 20% had 2‐vessel CAD, and 26% had 3‐vessel CAD. After adjusting for age, sex, race, body mass index, smoking, hypertension, diabetes mellitus history, and renal function, hsTnI levels were independently associated with the severity of CAD measured by the Gensini score (log 2 ß=0.31; 95% confidence interval, 0.18–0.44; P<0.001) and with CAD progression (log 2 ß=0.36; 95% confidence interval, 0.14–0.58; P=0.001). hsTnI level was also a significant predictor of incident death, cardiovascular death, myocardial infarction, revascularization, and cardiac hospitalizations, independent of the aforementioned covariates and CAD severity.ConclusionsHigher hsTnI levels are associated with the underlying burden of coronary atherosclerosis, more rapid progression of CAD, and higher risk of all‐cause mortality and incident cardiovascular events. Whether more aggressive treatment aimed at reducing hsTnI levels can modulate disease progression requires further investigation.

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“…For example, those individuals who exhibit MSIMI are more likely to be women, have greater microvascular disease, have poorer left ventricular dysfunction, and display endothelial dysfunction, whereas exercise/pharmacological stress-induced ischemia is generally associated with men and those with larger and more diffuse coronary artery plaque. [4][5][6] Though there are sex differences in the rates of presentations of both MSIMI and exercise/pharmacological stress-induced ischemia, both men and women do exhibit both of these forms of ischemia. However, we do not know if the mechanistic factors that underlie these stress-induced ischemia differ by sex; for example, does MSIMI in women differ from MSIMI in men?…”

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The Importance of Sex in the Stress–Heart Disease Relationship and the Potential Contribution of Gender to Future Research

Bacon

2018

ATVB

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We now have numerous studies that have linked increased levels of negative emotions and stress with the development and progression of cardiovascular disease-a relationship that seems to be sex specific in its pattern of outcomes. 1,2 However, the mechanisms of these relationships are still a source of much debate. One of the strongest potential pathways linking acute psychological stress with worse outcomes is through mental stress-induced myocardial ischemia (MSIMI).3 Though there is a large overlap (ca. 70%) in individuals who demonstrate both MSIMI and more common (ie, exercise or pharmacological) stress-induced ischemia, 4 these seem to be distinctly different entities. Firstly, it would seem that more individuals are likely to have MSIMI only than exercise/pharmacological stress-induced ischemia only (20% versus 10%).5 Furthermore, the profiles and potential mechanistic factors of those at risk for MSIMI compared with exercise/pharmacological stress-induced ischemia are different. For example, those individuals who exhibit MSIMI are more likely to be women, have greater microvascular disease, have poorer left ventricular dysfunction, and display endothelial dysfunction, whereas exercise/pharmacological stress-induced ischemia is generally associated with men and those with larger and more diffuse coronary artery plaque. [4][5][6] Though there are sex differences in the rates of presentations of both MSIMI and exercise/pharmacological stress-induced ischemia, both men and women do exhibit both of these forms of ischemia. However, we do not know if the mechanistic factors that underlie these stress-induced ischemia differ by sex; for example, does MSIMI in women differ from MSIMI in men? Understanding these processes can ultimately help in the development of better tailored diagnostic procedures and interventions to treat cardiovascular disease. See accompanying article on page 473The article by Sullivan et al 7 provides some important initial insights into sex differences in the potential mechanisms driving MSIMI. This secondary analysis of 678 (25% women) patients in the MIPS study (Mental Stress Ischemia Mechanisms and Prognosis) evaluated mental stress (public speaking)-induced vascular and hemodynamic responses. The authors found that MSIMI was generally driven by peripheral vasoconstriction in women compared with increased hemodynamic workload in men, results that were independent of exercise/pharmacological stress-induced ischemia. These results suggest that men with MSIMI are effectively cardiac stress reactors, with increased myocardial oxygen demands, and women with MSIMI are more likely to be vascular reactors, with greater endothelial driven increases in vascular resistance (which leads to increased left ventricular afterload and dysfunction).8 However, the article by Sullivan et al does only provide initial insights, and there is a great deal of further information that we need. For example, building a more complex map of MSIMI, to include additional measures of the autonomic nervous system, the...

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Association Between High-Sensitivity Cardiac Troponin Levels and Myocardial Ischemia During Mental Stress and Conventional Stress

Cited by 31 publications

References 35 publications

Coronary and Peripheral Vasomotor Responses to Mental Stress

Coronary and Peripheral Vasomotor Responses to Mental Stress

High‐Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long‐Term Outcomes

The Importance of Sex in the Stress–Heart Disease Relationship and the Potential Contribution of Gender to Future Research

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