Coronary calcium score is superior to exercise tolerance testing in predicting significant coronary artery stenosis

Bengrid, Tarek; Nicoll, Rachel; Zhao, Ying; Schmermund, Axel; Henein, Michael Y.

doi:10.1016/j.ijcard.2013.03.071

Cited by 3 publications

(3 citation statements)

References 11 publications

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“…As for the exact nature of that disease, we are unable to ascertain. The simplest arterial wall pathology that compromises coronary reserve is hardening of the wall, either due to calcium formation or collagen deposition (Asafu et al, 2018; Bengrid et al, 2013; Henein et al, 2016). In our patients, the strongest correlation with CAC score was TAPSE and RV s' in ICAD patients.…”

Section: Discussionmentioning

confidence: 99%

Longitudinal myocardial function is more compromised in cardiac syndrome X compared to insignificant CAD: Role of stress echocardiography and calcium scoring

Bytyçi

Bengrid

Henein

2021

Clin Physio Funct Imaging

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Background and Aim The aim of this study was to assess the nature of myocardial dysfunction in the cardiac syndrome X (CSX) and insignificant coronary artery disease (ICAD) using dobutamine stress echocardiography (DSE) and coronary calcium scoring (CAC). Methods We prospectively studied 35 consecutive patients who complained of exertional angina, had ≥1 mm ST shift on exercise stress test but normal or no obstructive CAD (<50%) on angiography. Patients were divided into CSX (n = 27) with normal arteries and ICAD (n = 8) with insignificant stenosis. Results CSX patients had more females, lower calcium score and less prevalent cardiac risk factors compared to ICAD (p < 0.05 for all). At peak stress, MAPSE and TAPSE failed to increase in both groups. LV septal and lateral s’ increased in the two groups but the increment increase was less in CSX than ICAD (p < 0.05) while other diastolic indices did not differ between groups (p > 0.05 for all). CAC correlated modestly with LV and RV systolic velocities: septal s' (r = −0.65, p < 0.001) lateral s' (r = −0.35, p = 0.04) and right s' (r = −0.53, p = 0.005) in CSX, while in ICAD patients only with RV s' (r = −0.58, p = 0.02). On multivariate model, only septal s' OR 1.816 (1.1090–3.820, p = 0.04) proved the most powerful independent predictor of CAC. Conclusions Compromised LV longitudinal systolic velocities were more pronounced and calcium score as a surrogate for atherosclerosis was lower in CSX than ICAD. These findings strengthen the evidence for different pathogenesis of CSX compared to ICAD, with microvascular disease in the former and calcification in the latter.

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Section: Discussionmentioning

confidence: 99%

Longitudinal myocardial function is more compromised in cardiac syndrome X compared to insignificant CAD: Role of stress echocardiography and calcium scoring

Bytyçi

Bengrid

Henein

2021

Clin Physio Funct Imaging

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“…Coronary artery calcification (CAC) is a well-recognized cause of arterial stiffness and develops with age, with its extent correlates with the severity of luminal stenosis in symptomatic patients. [2,3] Low-grade stenosis and extensive calcification in calcific coronary artery disease (CCAD) may also cause limiting symptoms due to compromised coronary flow reserve causing abnormal myocardial perfusion and hence generalized ischemia. [4,5] Such discrepancy in the expression pattern of coronary disease raises questions about the exact pathophysiology of coronary stiffness, particularly that caused by calcification, and whether there is a genetic etiology for it.…”

Section: Introductionmentioning

confidence: 99%

Genetic variants in cardiac calcification in Northern Sweden

2019

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Extensive coronary calcification without significant stenosis, described as calcific coronary artery disease (CCAD) may cause abnormal myocardial perfusion and hence generalized ischemia. There is a discrepancy in the expression pattern of CCAD compared to the well-known atherosclerotic disease which raises questions about the exact pathophysiology of coronary calcification and whether there is a genetic etiology for it. In this pilot study we studied 3 candidate genes, ectonucleotide pyrophosphatase/phosphodiesterase ( ENPP1 ), ATP Binding Cassette Subfamily C Member 6 ( ABCC6 ), and 5’-Nucleotidase Ecto ( NT5E ) involved in pyrophosphate (PP i ) and inorganic phosphate (P i ) metabolism, which may predispose to coronary arterial or valvular calcification. We studied 70 patients with calcific cardiac disease; 65 with CCAD (age 43–83 years) and 5 with calcific aortic valve disease (CAVD) (age 76–82 years). Five DNA variants potentially affecting protein function were found in 6 patients. One variant is a known disease-causing mutation in the ABCC6 gene. Our findings support that disturbances in the PP i and P i metabolism might influence the development of CCAD and CAVD. However, segregation in the families must first be performed to ascertain any damaging effect of these variants we have found. We report 4 new genetic variants potentially related to coronary calcification, through the disturbed P i and PP i metabolism. The search for direct causative genetic variants in coronary artery and aortic valve calcification must be broadened with other genes particularly those involved with P i and PP i metabolism.

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“…Coronary artery calcification (CAC) is the most common cause of arterial stiffness and it develops with age. The extent of CAC usually correlates with the severity of arterial lumen stenosis in symptomatic patients [1,2]. Low grade stenosis, however, may also be seen in a minority of patients with extensive calcification (calcific coronary artery disease, CCAD), in whom limiting symptoms can be explained on the basis of compromised coronary flow reserve causing abnormal myocardial perfusion and hence generalised ischaemia [3,4].…”

Section: Introductionmentioning

confidence: 99%

Is there a Role for Genetics in Cardiac Calcification?

Hellman¹,

Mörner²,

Henein³

2019

ICFJ

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Calcific coronary artery disease (CCAD) may cause abnormal myocardial perfusion and hence generalized ischaemia, despite potential discrepancy in its expression pattern compared to the well-known atherosclerotic disease which raises questions about the exact pathophysiology of coronary calcification and whether there is a genetic aetiology for it. In a pilot study we studied three candidate genes, ENPP1, ABCC6 and NTE5 which may predispose to coronary arterial or valvular calcification. We studied 65 patients with CCAD and 5 patients with calcific aortic valve disease (CAVD). Five DNA variants potentially affecting protein function were found in six patients. Our findings support genetic variants might influence the development of CCAD and CAVD, however, segregation in the families must first be performed to ascertain any damaging effect of these variants. The search for direct causative genetic variants in coronary artery and aortic valve calcification must be broadened with other genes.

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Coronary calcium score is superior to exercise tolerance testing in predicting significant coronary artery stenosis

Cited by 3 publications

References 11 publications

Longitudinal myocardial function is more compromised in cardiac syndrome X compared to insignificant CAD: Role of stress echocardiography and calcium scoring

Longitudinal myocardial function is more compromised in cardiac syndrome X compared to insignificant CAD: Role of stress echocardiography and calcium scoring

Genetic variants in cardiac calcification in Northern Sweden

Is there a Role for Genetics in Cardiac Calcification?

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