P3432Coronary artery calcium score is of limited sensitivity in detecting subclinical atherosclerosis in young individuals with family history of coronary artery disease

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A Huang ◽  
A Mugharbil ◽  
M Anastasius ◽  
S Ghadiri ◽  
J Leipsic ◽  
...  

Abstract Introduction Family history of premature coronary artery disease (CAD) is known to predispose individuals to adverse CAD events, often at a younger age. Current risk stratification strategy is suboptimal, as up to 50% of individuals were considered “low-risk” prior to their first presentation of myocardial infarction. Coronary artery calcium score (CACS) is a marker of atherosclerosis and provides incremental value in risk stratification. However, the utility of CACS may be limited in younger patients as they often have non-calcified atherosclerotic plaques. In this study, we evaluate the sensitivity of CACS in detecting subclinical atherosclerosis in different age groups. Method From 310 referrals to a specialized unit in the management of early atherosclerosis, 222 individuals with a family history of premature CAD (defined as CAD events in first-degree family members, male<55 and female<65) and aged between 35 and 55 were enrolled for assessment of their CAD risks. Individuals with possible, probably or definite familial hypercholesterolemia were excluded. In addition to clinical and risk factor evaluation, cardiac CT and CACS were performed in select individuals, at the discretion of the treating physician. Results Of the 141 (59% male, mean age 45.9±6.0 year) individuals that completed clinical evaluation, 65 (73% male, mean age 47.4±6.9 years) have subclinical atherosclerosis (defined by the presence of atherosclerotic plaques in any of the coronary artery segments in cardiac CT). Of them, 52 have CACS>0, giving an overall sensitivity of 80%. The breakdown by age group is shown in table 1. The sensitivity of CACS in detecting subclinical atherosclerosis is quite modest in younger individuals (60% in individuals <45 year-old) but improves with patient age (>85% in >45 years). Table 1. Sensitivity of CACS in different age groups Age group True Positive Fast Negative Sensitivity N (CAC+ CTCA+) (CAC+ CTCA−) (%) <40 6 4 60 10 41–45 7 4 55 11 46–50 19 3 86 22 51–55 20 1 95 21 Conclusion In younger individuals (<45 years) with family history of premature CAD, CACS is of limited sensitivity in detecting subclinical atherosclerosis, and should not be used to rule out CAD. Further studies are warranted.

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Ghadiri ◽  
J Leipsic ◽  
N Elahi ◽  
M Anastasius ◽  
A Huang ◽  
...  

Abstract Introduction Patients with family history of premature coronary artery disease (CAD) are at increased risk of CAD events at a younger age. Risk factor based approaches and clinical evaluation are most commonly used to assess these individuals. However, it has been recently shown that up to 50% of individual presenting with their first myocardial infarction (MI) were considered to be “low risk” prior to that event. MI is often a result of plaque rupture preceded by progression of subclinical atherosclerosis. Detection of subclinical atherosclerosis may therefore help target prevention of plaque progression. We assessed the value of clinical risk factor, biomarkers and Framingham Risk Score (FRS) in predicting subclinical atherosclerosis in individuals with a family history of premature CAD. Methods From 310 referrals, 222 individuals between the ages of 35 and 55 with a family history of premature CAD (CAD events in first-degree family members (male <55, female <65)) were enrolled for evaluation of risk of CAD. Those with familial hypercholesteremia (possible, probable or definite) were excluded. Patients underwent clinical and risk factor evaluations as well as Cardiac CT or Calcium Score (CS) to assess presence of subclinical / clinical atherosclerosis at the discretion of the treating physician. Results In this pilot, 141 individuals (59% male, mean age 45.9±6.0 years) completed evaluation, and 65 (46%) had evidence of subclinical atherosclerosis on CT coronary angiography or CT calcium score with a mean segment involvement score (SIS) of 2.8 and mean CS of 152, putting them above the 80th percentile for their age and sex. Aside from male sex, age, and smoking history, other traditional risk factors and biomarkers including diabetes mellitus, hypertension, total cholesterol, LDL-C, HDL-C and Cholesterol/HDL-C were not significantly different between those with or without subclinical atherosclerosis (Table 1). Table 1 Conclusion In young individuals with a family history of premature CAD, risk factors, biomarkers, and FRS failed to identify individuals with premature, subclinical atherosclerosis in this pilot study. Detection of subclinical atherosclerosis and early implementation of treatment with the aim of stabilizing plaques and stopping progression might prove vital in reducing events in these individuals. Further studies are warranted.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Ahmed Abdi Ali ◽  
Abdel Aziz Shaheen ◽  
Danielle A Southern ◽  
Mei Zhang ◽  
Merril Knudston ◽  
...  

Background: Family history (FHx) of premature coronary artery disease (CAD) is an established cardiovascular risk factor. However the impact of FHx on outcomes of patients with CAD is unclear. Methods & Results: The Alberta Provincial Project for Outcomes Assessment in Coronary Heart Disease (APPROACH) Program is an inclusive prospective registry of patients undergoing coronary angiography. Between April 2002 and Mar 2013, 99,667 patients were enrolled. 30,030 (30%) patients reported FHx, defined as a first degree relative with premature CAD (males <55, females <65 years). We investigated the association between FHx and all-cause mortality at 1 year, using multivariable logistic regression, adjusting for clinical characteristics, comorbidities, and the extent of CAD. Patients with normal angiography (15.2%) were excluded. Compared to those without FHx, those with FHx were younger (60.1 vs 64.0 years, p<0.0001), more likely female (30.5% vs 29.5%; p=0.0018), and were less likely to have previously diagnosed CAD, congestive heart failure, stroke, or chronic kidney disease (all p<0.0001) Conversely, those with FHx were more likely current smokers (31.8% vs 25.3%) and to have hypertension (68.8% vs 65.5%) and dyslipidemia (75.7% vs 68.1%), all p<0.0001). The indication for angiography was an acute coronary syndrome (ACS) in 55% of both groups (p=0.57), and the extent of CAD was similar. Overall, FHx was associated with reduced 1-year mortality in fully adjusted models (odds ratio [OR] 0.56, 95% CI 0.51 to 0.62). This protective association was present in patients with and without a previous CAD event (OR 0.66 [95% CI 0.60 to 0.78] vs 0.53 [95% CI 0.47 to 0.59], respectively), and in patients with and without an ACS (OR 0.56 [95% CI 0.50 to 0.63] vs 0.56 [95% CI 0.48 to 0.65], respectively). There was slight attenuation of association with age, but FHx remained protective even in those aged 80 or more (OR 0.72, 95% CI 0.57 to 0.90). Conclusion: In patients with angiographic CAD, a family history of premature CAD is associated with lower mortality, independent of clinical characteristics, mode of presentation, and extent of disease. Further investigation of potential patient- and system-level mediators of this seemingly paradoxical relationship is required.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Muhammad Hammadah ◽  
Riyaz S Patel ◽  
Danny J Eapen ◽  
Ayman Samman Tahhan ◽  
Nima Ghasemzadeh ◽  
...  

Introduction: A family history (FH) of premature coronary artery disease (CAD) is an important prognostic risk factor. Emerging evidence suggests that CAD location as well as severity may be heritable. We sought to investigate the association between a FH of premature CAD with the location and severity of angiographically phenotyped CAD. Methods: 2854 patients undergoing coronary angiography were enrolled from the Emory Cardiovascular Biobank. A FH of CAD was defined as having any male or female relative with history of CAD at age ≤55 or ≤65 year old respectively. Coronary angiograms were phenotyped using a 17 segment AHA model. Proximal disease was defined as having ≥70% lesion in the left main or proximal portion of any of the three major epicardial arteries, while CAD severity was assessed by counting the number of vessels with ≥70% stenosis. Results: Among this population (mean age 63±12, male 67%, diabetes 33%), 21% reported a positive FH of premature CAD. After adjustment for age, gender, and traditional cardiovascular risk factors, those with a positive FH were more likely to have significant CAD than those without a positive FH (OR 1.3 (1.1-1.7)). They were 40% more likely to have single vessel (OR 1.4(1.1-1.7)) and up to 80% more likely to have multi-vessel disease (OR 1.8 (1.4-2.4)). In addition, they were also much more likely to have left main (OR 1.9 (1.3-2.8)) and proximal vessel involvement (OR 1.5 (1.2 - 1.9)), but not distal vessel stenosis (OR 1.1 (0.9-1.4)). Conclusions: A FH of CAD is associated with a greater likelihood of multi-vessel and proximal anatomical disease. Whether site specific disease is genetically mediated remains to be explored.


2008 ◽  
Vol 155 (6) ◽  
pp. 1020-1026.e1 ◽  
Author(s):  
Catalin Taraboanta ◽  
Evelyn Wu ◽  
Scott Lear ◽  
Stefanie DiPalma ◽  
John Hill ◽  
...  

Author(s):  
Unnikrishnan Kartha T. D. ◽  
Ambili N. R. ◽  
Donna Mathew ◽  
Renymol B.

Background: Coronary artery disease is becoming the leading cause of death in the world. The incidence of CAD in females has increased rapidly in the past decades. This study aimed to analyze the clinical profile of premenopausal women with CAD and elucidate on the possible risk factors.Methods: Premenopausal female patients admitted with an acute coronary syndrome as diagnosed by history, ECG and laboratory tests were recruited. Clinical and biochemical parameters were recorded.Results: Mean age of study participants was 41.6±8.18 yrs. Unstable angina (60%) was the most common clinical presentation. Proportion of women with various risk factors of CAD in our study population were as follows dyslipidemia (65%), family history of premature CAD (57.5%), hypertension (55%), diabetes mellitus (42.5%), hypothyroidism (40%), PAD (37.5%), CKD (35%) and SLE (20%). Most (95%) of the study population had high LDL-c. Three fourth (77.5%) of the study population had low HDL Approximately half of the study population had fatty liver on ultrasonography. Triglyceridemia was found in 72.5% of the study population.Conclusions: Premature CAD is increasingly evident in young premenopausal women in India. Premenopausal CAD in India is of multi factorial causation and dyslipidemia, hypertension, diabetes mellitus, central obesity and family history of premature CAD play a crucial role in its development.


2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Hamza Rana ◽  
Jeanette S Andrews ◽  
Kimberley J Hansen ◽  
Pavel J Levy

Objective: Premature atherosclerotic peripheral artery disease (PAD) is being diagnosed with increasing frequency. Little is known about concomitant coronary artery disease (CAD) in patients with premature PAD. This study examines prevalence, associated clinical characteristics, and predictors of concomitant CAD in young PAD patients. Methods: We studied patients with severe atherosclerotic PAD <55 years of age (mean 49.36±6.45 yrs) treated at a single academic Vascular center between 1998 and 2010. Data was collected at the time of initial evaluation. CAD was defined by documented acute coronary syndrome; and/or prior coronary revascularizations. Associations with concomitant CAD were evaluated univariately using chi-square tests for categorical characteristics or t-tests for continuous characteristics, and using multivariable logistic regression. Results: Total of 561 patients (46% female, 20% Black) were analyzed. Mean age at diagnosis was 46.64±6.86 years. Risk factors included smoking (97%), hyperlipidemia (67%), hypertension (64%), family history of premature CAD (47%), and diabetes (25%). Aortoiliac disease was present in 77% of patients; 36% were disabled. Overall, 174 (31%) patients had clinical CAD. Patients with premature CAD were less likely to be Blacks (p=0.004), had greater frequency of hypertension, hyperlipidemia, diabetes, family history of premature CAD, polyvascular disease (i.e. cerebral vascular disease [CeVD]) (p<.001 for each), renovascular disease (p=.016) and mesenteric disease (p=.012). Multivariable logistic regression modeling showed higher odds of concomitant CAD for patients with hyperlipidemia (OR 4.71; 95 CI 2.82-7.85; p<.0001), diabetes (OR 2.11; 95% CI 1.28-3.47; p<0.01), family history of premature CAD OR 2.00; 95% CI 1.27-3.14;p<0.01) CeVD (OR 2.15; 95% CI 1.34-3.48;p<0.01), mesenteric vascular disease (OR 2.70;95% CI 1.19-6.14; p=.02). One pack year in smoking increase had 1.01 times odds of concomitant CAD (95% CI 1.001-1.018; p=.02). Conclusions: Clinical CAD was prevalent in 1/3 of patients with premature PAD, and those with premature CAD were less likely to be Black. Among patients with premature PAD, higher odds of concomitant clinical CAD were associated with presence of hyperlipidemia, diabetes, family history of premature CAD, polyvascular disease.


2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
D Vikulova ◽  
L Bevanda ◽  
S N Pimstone ◽  
L R Brunham

Abstract Background Premature atherosclerotic cardiovascular disease (ASCVD) is highly heritable. The screening of first-degree relatives (FDR) of patients with premature ASCVD is recommended but not routinely performed, and the diagnostic yield of different approaches to such screening is unknown. Purpose To determine the feasibility and diagnostic yield of clinical and radiological screening of FDRs of patients with premature coronary artery disease (CAD) in clinical setting. Method We recruited FDRs of patients with angiographically-proven CAD with stenosis of ≥50% who presented at the age of ≤50 years for males and ≤55 years for females. After clinical and laboratory assessment, patients with no personal history of cardiovascular disease underwent either coronary computed tomography angiography (CCTA), coronary calcium scoring assessment (CAC), or carotid ultrasound (CUS). Subclinical atherosclerosis was defined as 1) CAC score &gt;100 Agatston units or &gt;75% percentile for age and sex; 2) Stenosis &gt;50% in at least one coronary artery or segment involvement scores &gt;50th percentile in males and &gt;75th in females; or, 3) Carotid plaque on ultrasonography. Results We enrolled 220 FDRs between 2017 and 2020, 129 completed clinical assessment (Figure 1). Of them, 28 (21.7%) had a personal history of ASCVD and 101 were tested for subclinical atherosclerosis. The characteristics of these patients are shown in Table 1. The most prevalent cardiovascular risk factors were dyslipidemia (40.6%), hypertension (22.8%), and obesity (21.8%). When assessed with the Framingham risk score calculator without adjustment for family history, only 5.1% and 28.6%, of patients had high or moderate cardiovascular risk, respectively. After adjusting for family history and the presence of statin-indicated conditions, 39.6% and 14.9% of patients were placed in high and moderate risk groups, respectively. Subclinical atherosclerosis was found in 43.6% of all patients (Figure 1) and 57.7% of patients over 40 years of age. The diagnostic yield of procedures was 29.6% for CUS, 37.8% for CCTA and 61.1% for CAC scoring. After the radiological assessment, 13.9% of patients were reclassified to a higher risk group (Table 1). Conclusion Non-invasive cardiovascular imaging detected subclinical atherosclerosis in 43.6% of healthy patients with a family history of premature ASCVD, moving 1 in 7 patients to a higher risk group and suggesting that this screening approach may improve risk prediction in this population. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Canadian Institutes of Health Research.St. Paul's Hospital Foundation and the Vancouver General Hospital Foundation. Figure 1 Table 1


Sign in / Sign up

Export Citation Format

Share Document