scholarly journals Secondary prevention patterns in persons with pre-existing coronary artery disease: Are we getting it right?

2017 ◽  
Vol 27 (3) ◽  
pp. 157-161
Author(s):  
Muhammad Imran Abdul Hafidz ◽  
Lily Diana Zainudin ◽  
Zhen-Vin Lee ◽  
Mohd Firdaus Hadi ◽  
Ahmad Syadi Mahmood Zuhdi
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
High Risk ◽  
Secondary Prevention ◽  
Lipid Lowering ◽  
Lipid Lowering Therapy ◽  
Increased Risk ◽  
Artery Disease ◽  
High Risk Cohort

Background: Cardiovascular diseases are the main cause of death globally. Individuals with evidence of coronary artery disease are at increased risk of further cardiovascular events. However, with good secondary prevention, which consists broadly of lifestyle changes, medical therapy and revascularisation, this risk can be reduced. The true extent of secondary prevention in individuals who are re-admitted with a myocardial infarction in such a high-risk cohort has never been explored in Malaysia. Methods: We performed a retrospective, observational study in a tertiary hospital in 100 individuals with previously diagnosed coronary artery disease admitted with a myocardial infarction from August 2016 to February 2017. Results: Twenty-nine per cent of patients were still smoking; 15% and 47% were not taking antiplatelet or beta-blocker therapy, respectively. A further 45% and 20% of patients were not on any renin–angiotensin–aldosterone inhibition or lipid-lowering therapy, respectively. Conclusion: In our high-risk cohort, secondary prevention practices were sub-optimal. Poor physician–patient communication was frequently listed as a major factor. Simple strategies taken at various levels of care should be implemented and audited to improve these practices.

scholarly journals Dual Antiplatelet or Dual Antithrombotic Therapy for Secondary Prevention in High-Risk Patients with Stable Coronary Artery Disease?

2019 ◽  
Vol 119 (10) ◽  
pp. 1583-1589 ◽  
Author(s):  
Wael Sumaya ◽  
Tobias Geisler ◽  
Steen D. Kristensen ◽  
Robert F. Storey
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
High Risk ◽  
Secondary Prevention ◽  
Dual Antiplatelet Therapy ◽  
Stable Coronary Artery Disease ◽  
Risk Patients ◽  
History Of ◽  
Artery Disease

AbstractAntithrombotic treatment is a key component of secondary prevention following acute coronary syndromes (ACS). Although dual antiplatelet therapy is standard therapy post-ACS, duration of treatment is the subject of ongoing debate. Prolonged dual antiplatelet therapy in high-risk patients with history of myocardial infarction reduced the risk of recurrent myocardial infarction, stroke or cardiovascular death. Similarly, in patients with stable coronary artery disease, two-thirds of whom had a history of myocardial infarction, dual antithrombotic therapy with very-low-dose rivaroxaban and aspirin also resulted in improved ischaemic outcomes. In the absence of head-to-head comparison, choosing the most appropriate treatment strategy can be challenging, particularly when it comes to balancing the risks of ischaemia and bleeding. We aim to review the evidence for currently available antithrombotic treatments and provide a practical algorithm to aid the decision-making process.

scholarly journals Coronary lesion complexity in patients with heterozygous familial hypercholesterolemia hospitalized for acute myocardial infarction: data from the RICO survey

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Hermann Yao ◽  
Michel Farnier ◽  
Laura Tribouillard ◽  
Frédéric Chague ◽  
Philippe Brunel ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
High Risk ◽  
Ldl Cholesterol ◽  
Statin Treatment ◽  
Lipid Lowering ◽  
Syntax Score ◽  
Lipid Lowering Therapy ◽  
Lipid Clinic ◽  
Acute Mi ◽  
Artery Disease

Abstract Background Although patients with familial heterozygous hypercholesterolemia (FH) have a high risk of early myocardial infarction (MI), the coronary artery disease (CAD) burden in FH patients with acute MI remains to be investigated. Methods The data for all consecutive patients hospitalized in 2012–2019 for an acute MI and who underwent coronary angiography were collected from a multicenter database (RICO database). FH (n = 120) was diagnosed using Dutch Lipid Clinic Network criteria (score ≥ 6). We compared the angiographic features of MI patients with and without FH (score 0–2) (n = 234) after matching for age, sex, and diabetes (1:2). Results Although LDL-cholesterol was high (208 [174–239] mg/dl), less than half of FH patients had chronic statin treatment. When compared with non-FH patients, FH increased the extent of CAD (as assessed by SYNTAX score; P = 0.005), and was associated with more frequent multivessel disease (P = 0.004), multiple complex lesions (P = 0.022) and significant stenosis location on left circumflex and right coronary arteries. Moreover, FH patients had more multiple lesions, with an increased rate of bifurcation lesions or calcifications (P = 0.021 and P = 0.036, respectively). In multivariate analysis, LDL-cholesterol levels (OR 1.948; 95% CI 1.090–3.480, P = 0.024) remained an independent estimator of anatomical complexity of coronary lesions, in addition to age (OR 1.035; 95% CI 1.014–1.057, P = 0.001). Conclusions FH patients with acute MI had more severe CAD, characterized by complex anatomical features that are mainly dependent on the LDL-cholesterol burden. Our findings reinforce the need for more aggressive preventive strategies in these high-risk patients, and for intensive lipid-lowering therapy as secondary prevention.

Abstract 18995: Statins in Familial Hypercholesterolemia - Effects on Coronary Artery Disease and All-cause Mortality

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Joost Besseling ◽  
Gerard K Hovingh ◽  
John J Kastelein ◽  
Barbara A Hutten
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Familial Hypercholesterolemia ◽  
Lipid Lowering ◽  
Premature Coronary Artery Disease ◽  
Lipid Lowering Therapy ◽  
Time Varying ◽  
All Cause Mortality ◽  
Artery Disease

Introduction: Heterozygous familial hypercholesterolemia (heFH) is characterized by high levels of low-density lipoprotein cholesterol (LDL-C) and increased risk for premature coronary artery disease (CAD) and death. Reduction of CAD and mortality by statins has not been properly quantified in heFH. The aim of the current study is to determine the effect of statins on CAD and mortality in heFH. Methods: All adult heFH patients identified by the Dutch FH screening program between 1994 and 2014 and registered in the PHARMO Database Network were eligible. Of these patients we obtained hospital, pharmacy (in- and outpatient), and mortality records in the period between 1995 and 2015. The effect of statins (time-varying) on CAD and all-cause mortality was determined using a Cox proportional hazard model, while correcting for the use of other lipid-lowering therapy, thrombocyte aggregation inhibitors, antihypertensive and antidiabetic medication (all time-varying). Furthermore, we used inverse probability for treatment weighting (IPTW) to account for differences between statin-treated and untreated patients regarding history of CAD before follow-up, age at start of follow-up and age of screening, as well as body mass index, LDL-C and triglycerides. Results: Of the 25,479 identified heFH patients, 11,021 gave informed consent to obtain their medical records, of whom 2,447 could be retrieved. We excluded 766 patients younger than 18. The remaining 1,681 heFH patients comprised our study population and these had very similar characteristics as compared to the 23,798 excluded FH patients, e.g. mean (SD) LDL-C levels were 214 (74) vs. 203 (77) mg/dL. Among 1,151 statin users, there were 133 CAD events and 15 deaths during 10,115 statin treated person-years, compared to 17 CAD events and 9 deaths during 4,965 person-years in 530 never statin users (combined rate: 14.6 vs. 5.2, respectively, p<0.001). After applying IPTW to account for indication bias and correcting for use of other medications, the hazard ratio of statin use for CAD and all-cause mortality was 0.61 (0.40 - 0.93). Conclusions: In heFH patients, statins lower the risk for CAD and mortality by 39%.

Abstract P380: Coronary Artery Disease Extent is Predictive of Heart Failure Incidence After Myocardial Infarction

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Yariv Gerber ◽  
Susan A Weston ◽  
Maurice E Sarano ◽  
Sheila M Manemann ◽  
Alanna M Chamberlain ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Proportional Hazards ◽  
Incidence Rates ◽  
Cox Proportional Hazards ◽  
Disease Extent ◽  
Increased Risk ◽  
Artery Disease

Background: Little is known about the association between coronary artery disease (CAD) and the risk of heart failure (HF) after myocardial infarction (MI), and whether it differs by reduced (HFrEF) or preserved (HFpEF) ejection fraction (EF) has yet to be determined. Subjects and Methods: Olmsted County, Minnesota residents (n=1,924; mean age, 64 years; 66% male) with first MI diagnosed in 1990-2010 and no prior HF were followed through 2013. Framingham Heart Study criteria were used to define HF, which was further classified according to EF (applying a 50% cutoff). The extent of angiographic CAD was defined at index MI according to the number of major epicardial coronary arteries with ≥50% lumen diameter obstruction. Fine & Gray and Cox proportional hazards regression models were used to assess the association of CAD categories with incidence of HF, and multiple imputation methodology was applied to account for the 19% with missing EF data. Results: During a mean (SD) follow-up of 6.7 (5.9) years, 594 patients developed HF. Adjusted for age and sex, with death considered a competing risk, the cumulative incidence rates of HF among patients with 1- (n=581), 2- (n=622), and 3-vessel disease (n=721) were 11.2%, 14.6% and 20.5% at 30 days; and 18.1%, 22.3% and 29.4% at 5 years after MI, respectively. The increased risk of HF with greater number of occluded vessels was only modestly attenuated after further adjustment for patient and MI characteristics, and did not differ materially by EF (Table). Conclusions: The extent of angiographic CAD expressed by the number of diseased vessels is independently associated with HF incidence after MI. The association is evident promptly after MI and applies to both HFrEF and HFpEF.

P5508Impact of CD14++CD16+ monocytes on coronary plaque vulnerability assessed by optical coherence tomography in coronary artery disease patients

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Yamamoto ◽  
H Otake ◽  
T Shinke ◽  
T Yamashita ◽  
H Kawamori ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Coronary Plaque ◽  
Lipid Lowering ◽  
Lipid Lowering Therapy ◽  
Plaque Vulnerability ◽  
Glucose Fluctuation ◽  
Fibrous Cap ◽  
Lipid Rich Plaque ◽  
Artery Disease

Abstract Background Diabetes mellitus has been known as an important factor of coronary artery disease (CAD) progression despite of widespread with lipid-lowering therapy. Although we have reported that large glucose fluctuation is associated with the development of cardiovascular disease in both diabetes mellitus (DM) and non-DM patients, the underlying mechanisms remain unclear. Monocytes play a key role for atherosclerotic plaque formation. Monocytes in human peripheral blood are divided into three subsets: CD14++CD16− monocytes, CD14++CD16+ monocytes, and CD14+CD16++ monocytes. The CD14++CD16+ monocyte subset has recently received attention because it is reported to be associated with future cardiovascular events such as acute myocardial infarction. However, their impact on coronary plaque vulnerability in coronary artery disease (CAD) patients with or without DM remains unclear. Purpose The aim of this study was to investigate the impact of CD14++CD16+ monocyte levels on coronary plaque vulnerability and glucose fluctuation in stable CAD patients with well-regulated lipid levels. Methods This prospective observational study included 50 consecutive patients with CAD (DM [n=22], Non-DM [n=28]), receiving lipid-lowering therapy and undergoing coronary angiography and optical coherence tomography (OCT). Patients were divided into 3 tertiles according to the CD14++CD16+ monocyte percentages assessed by flow cytometry. Standard OCT parameters including lipid arc, lipid length, fibrous cap thickness (FCT) on lipid rich plaque, were assessed for 97 angiographically intermediate lesions (diameter stenosis: 30–70%). The presence of thin-cap fibroatheroma (TCFA), defined as a thin fibrous cap (<65μm) overlying a lipid-rich plaque (>90°), was also assessed. Daily glucose fluctuation assessed by using continuous glucose monitoring system was analyzed by measuring the mean amplitude of glycemic excursion (MAGE). Results CD14++CD16+ monocytes negatively correlated with FCT on lipid rich plaque (r=0.508, p<0.01) (Figure. 1). The presence of thin-cap fibroatheroma (TCFA) was increased stepwise according to the tertile of CD14++CD16+ monocytes (0 [tertile 1] vs. 5 [tertile 2] vs. 10 [tertile 3], p<0.01). CD14++CD16+ monocytes were a significant determinant of TCFA (OR 1.279, p=0.001). Although CD14++CD16+ monocytes were not significantly correlated with MAGE in DM patients (r=0.259, p=0.244), a significant relationship was found between CD14++CD16+ monocytes and MAGE in non-DM patients (r=0.477, p=0.018) (Figure 2). Conclusions CD14++CD16+ monocytes were associated with coronary plaque vulnerability in CAD patients with well-regulated lipid levels both in DM and non-DM patients. Cross-talk between glucose fluctuation and CD14++CD16+ monocytes may enhance plaque vulnerability, particularly in non-DM patients. CD14++CD16+ monocytes could be a possible therapeutic target for coronary plaque stabilization.

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