Documented History Of Coronary Artery Disease Research Articles

Romanian Patients Who Experience in-Stent Restenosis After St-Elevation Myocardial Infarction: The Experience of a Tertiary Center

Abstract Background and aim. Coronary artery disease (CAD) is one of the most important causes of death worldwide. ST-elevation myocardial infarction (STEMI) is an acute form of presentation in patients with CAD. Percutaneous coronary intervention (PCI) is the treatment of choice in STEMI patients. Generally, a stent is placed after the culprit lesion is dilated in order to ensure the patency of the coronary artery. In-stent restenosis (ISR) is a possible chronic complication in this setting. The following study is one of the few of its kind, since it investigates ISR in a cohort of Romanian patients who underwent PCI in the setting of STEMI. Our current descriptive study aims at highlighting the characteristics of these patients and identifying potential risk factors in this specific population, which could be validated by a further larger study. Methods. We studied 68 patients from “Dr. Carol Davila” Central Military Emergency University Hospital in Bucharest, Romania, who presented with STEMI in 2016. The mean time for angiographic reevaluation was 111 days. Results. 94% (64) of the patients underwent primary PCI, while in 6% (4) of the cases thrombolysis was initially attempted before PCI. The most prevalent risk factors that we identified were: arterial hypertension (61%), dyslipidemia (60%) and smoking or history of smoking (47%). The anterior myocardial infarction was the most prevalent (49%). Only 6% of the patients had a documented history of CAD, while on the other hand chronic occlusions were observed in most patients (85%). Of note is that only 11% of the patients reported recurrent angina before the angiographic reevaluation. Conclusion. Common cardiovascular risk factors are also involved in ISR. Their poor management in the case of Romanian patients with STEMI increases the risk of ISR. The lack of symptoms in patients with ISR constitutes a warning sign for clinicians and shows that ISR is a complication which can be easily omitted. Therefore, its incidence is probably underestimated.

Aspirin resistance: Prevalence and clinical outcome in Egypt

IntroductionThe antiplatelet drug aspirin is considered as a cornerstone in medical treatment of patients with CV or cerebrovascular diseases. Despite its use, a significant number of patients had recurrent adverse ischemic events. Inter-individual variability of platelet aggregation in response to aspirin may be an explanation for some of these events. Multiple trials have linked aspirin resistance to these adverse events. ObjectivesThe aim of this study was to estimate the prevalence of aspirin resistance among patients with coronary artery disease (CAD) in Egypt and evaluate its impact on clinical outcome. MethodsA total of 50 patients with documented history of CAD were included; they were on aspirin 150mg/day for more than seven days and no other antiplatelet drugs. They were evaluated for aspirin resistance using light transmission aggregometry. Aspirin resistance was defined as a mean aggregation of >20% with 0.5mg/ml arachidonic acid. They were followed up after six months for cardiac death, unstable angina (UA), myocardial infarction (MI), and stroke. ResultsPrevalence of aspirin resistance was 48% in our study group. Aspirin resistance was significantly higher in patients with family history of CAD (p=0.044), smoking (p=0.011), history of MI (p=0.024), history of percutaneous coronary intervention (PCI) (p=0.001), and concomitant NSAIDs intake (p=0.047). Moreover, aspirin resistance was more common among patients with multi-vessel CAD (p=0.024). Aspirin-resistant patients had a significantly higher rate of UA (p=0.001) and all major adverse cardiac events (MACE) (p<0.001).

Quantitative relationship between coronary artery calcium score and hyperemic myocardial blood flow as assessed by hybrid 15O-water PET/CT imaging in patients evaluated for coronary artery disease

BackgroundThe incremental value of CAC over traditional risk factors to predict coronary vasodilator dysfunction and inherent myocardial blood flow (MBF) impairment is only scarcely documented (MBF). The aim of this study was therefore to evaluate the relationship between CAC content, hyperemic MBF, and coronary flow reserve (CFR) in patients undergoing hybrid 15O-water PET/CT imaging.MethodsWe evaluated 173 (mean age 56 ± 10, 78 men) patients with a low to intermediate likelihood for coronary artery disease (CAD), without a documented history of CAD, undergoing vasodilator stress 15O-water PET/CT and CAC scoring. Obstructive coronary artery disease was excluded by means of invasive (n = 44) or CT-based coronary angiography (n = 129).Results91 of 173 patients (52%) had a CAC score of zero. Of those with CAC, the CAC score was 0.1-99.9, 100-399.9, and ≥400 in 31%, 12%, and 5% of patients, respectively. Global CAC score showed significant inverse correlation with hyperemic MBF (r = −0.32, P < .001). With increasing CAC score, there was a decline in hyperemic MBF on a per-patient basis [3.70, 3.30, 2.68, and 2.53 mL · min−1 · g−1, with total CAC score of 0, 0.1-99.9, 100-399.9, and ≥400, respectively (P < .001)]. CFR showed a stepwise decline with increasing levels of CAC (3.70, 3.32, 2.94, and 2.93, P < .05). Multivariate analysis, including age, BMI, and CAD risk factors, revealed that only age, male gender, BMI, and hypercholesterolemia were associated with reduced stress perfusion. Furthermore, only diabetes and age were independently associated with CFR.ConclusionIn patients without significant obstructive CAD, a greater CAC burden is associated with a decreased hyperemic MBF and CFR. However, this association disappeared after adjustment for traditional CAD risk factors. These results suggest that CAC does not add incremental value regarding hyperemic MBF and CFR over established CAD risk factors in patients without obstructive CAD.

Carotid artery intima-media thickness, but not coronary artery calcium, predicts coronary vascular resistance in patients evaluated for coronary artery disease

There is growing evidence that coronary artery disease (CAD) affects not only the conduit epicardial coronary arteries, but also the microvascular coronary bed. Moreover, coronary microvascular dysfunction (CMVD) often precedes the stage of clinically overt epicardial CAD. Coronary artery calcium (CAC) and carotid intima-media thickness (C-IMT) measured with computed tomography (CT) and ultrasound, respectively, are among the available techniques to non-invasively assess atherosclerotic burden. An increased CAC score and C-IMT have also been associated with CMVD. It is therefore of interest to explore and compare the potential of CAC against C-IMT to predict minimal coronary vascular resistance (CVR). We evaluated 120 patients (mean age 56 ± 9 years, 58 men) without a documented history of CAD in whom obstructive CAD was excluded. All patients underwent C-IMT measurements, CAC scoring, and vasodilator stress (15)O-water positron emission tomography (PET)/CT, during which the coronary flow reserve (CFR) and minimal CVR were analysed. Minimal CVR increased significantly with increasing tertiles of C-IMT (22 ± 6, 27 ± 11, and 28 ± 9 mmHg mL(-1)min(-1) g(-1), P < 0.01), whereas the CFR was comparable across all C-IMT groups (P = 0.50). Minimal CVR increased significantly with an increase in CAC score (23 ± 9, 27 ± 8, 32 ± 10, and 32 ± 7 mmHg mL(-1) min(-1) g(-1), P < 0.01), whereas the CFR did not show a significant decrease with higher CAC scores (P = 0.18). Multivariable regression analysis revealed that C-IMT (P = 0.03), but not CAC, was independently associated with minimal CVR. C-IMT, but not CAC score, independently predicts minimal CVR in patients with multiple cardiovascular risk factors and suspected of CAD.

Association of endothelial dysfunction with endothelin, nitric oxide and eNOS Glu298Asp gene polymorphism in coronary artery disease.

The endothelial dysfunction has been implicated as a major event in the pathogenesis of atherosclerosis. Therefore, this study was planned to determine (a) role of endothelium-derived nitric oxide (NO) and endothelin as coronary artery disease (CAD) risk markers and (b) intergenotypic variation of endothelial nitric oxide synthase (eNOS) Glu298Asp polymorphism in CAD.The endothelin, NO and eNOS genotypes were determined in 60 patients with documented history of CAD. These were compared with 50 age- and sex- matched healthy controls. The genotype frequencies for eNOS gene polymorphism were determined by PCR and RFLP. The plasma endothelin in CAD patients was significantly higher (p < 0.001) whereas, the NO level in CAD group was significantly lower (p < 0.001) than the control group. The genotype frequencies for Glu298/Asp (Glu/Glu and Glu/Asp) genotypes were 75% and 25% in CAD subjects and 88% and 12% in control subjects, respectively. No Asp/Asp was found in any of the groups. The genotype frequencies differed significantly (p < 0.05) between the controls and cases. In conclusion, endothelin and NO may be used as markers of endothelial dysfunction in CAD. Asp allele might be a risk factor for CAD in the North Indian population.

Association of Endothelial Dysfunction with Endothelin, Nitric Oxide and eNOS Glu298Asp Gene Polymorphism in Coronary Artery Disease

The endothelial dysfunction has been implicated as a major event in the pathogenesis of atherosclerosis. Therefore, this study was planned to determine (a) role of endothelium-derived nitric oxide (NO) and endothelin as coronary artery disease (CAD) risk markers and (b) intergenotypic variation of endothelial nitric oxide synthase (eNOS) Glu298Asp polymorphism in CAD.The endothelin, NO and eNOS genotypes were determined in 60 patients with documented history of CAD. These were compared with 50 age- and sex- matched healthy controls. The genotype frequencies for eNOS gene polymorphism were determined by PCR and RFLP. The plasma endothelin in CAD patients was significantly higher (p&lt; 0.001) whereas, the NO level in CAD group was significantly lower (p&lt; 0.001) than the control group. The genotype frequencies for Glu298/Asp (Glu/Glu and Glu/Asp) genotypes were 75% and 25% in CAD subjects and 88% and 12% in control subjects, respectively. No Asp/Asp was found in any of the groups. The genotype frequencies differed significantly (p&lt; 0.05) between the controls and cases. In conclusion, endothelin and NO may be used as markers of endothelial dysfunction in CAD. Asp allele might be a risk factor for CAD in the North Indian population.

Prevalence of silent myocardial ischemia in single and multiple lacunar infarcts and large vessel disease stroke

Background and purpose The relationships between single (SLI) and multiple lacunar infarcts (MLI) and occult coronary artery disease (CAD) have not yet been sufficiently evaluated. We aimed to investigate the prevalence of silent CAD in patients with SLI, MLI and large vessel disease (LVD) stroke, and to identify factors associated with its presence. Methods We enrolled 125 patients who had suffered their first non-cardioembolic ischemic stroke but had no documented history of CAD. According to their pathologies, these patients were assigned to one of three groups: MLI ( n = 21), SLI ( n = 50) or LVD ( n = 54). Asymptomatic CAD was detected by myocardial perfusion SPECT imaging. Results Silent CAD was detected in 40 patients (32% of the total); of those that experienced CAD, 15 (30%) were from the SLI group, 7 (33%) had MLI, and 18 (33%) had an LVD stroke. Differences between the groups were not significant. During a median follow-up of 48 months, the overall stroke recurrence was 8.8%; the stroke recurrence rates for each subgroup were 6% in patients with SLI, 7% in LVD and 19% in MLI. Mortality was higher in patients from the MLI and LVD groups (26% and 14%, respectively) than in those from the SLI group (6%; p = 0.02). We found no relationships between the various risk factors and silent CAD. Conclusions In this exploratory study, SPECT imaging results revealed that the prevalence of abnormal myocardial perfusion was similar in patients with either single or multiple lacunar infarcts and those that had experienced large vessel disease stroke.

Comparison of Peripheral Arterial Response to Mental Stress in Men Versus Women With Coronary Artery Disease

There are profound gender-related differences in the incidence, presentation, and outcomes of coronary artery disease (CAD). These differences are not entirely explained by traditional cardiovascular risk factors. Nontraditional risk factors, such as psychological traits, have increasingly been recognized as important contributors to the genesis and outcomes of CAD. Mental stress induces significant peripheral arterial vasoconstriction, with consequent increases in heart rate and blood pressure. These changes are thought to underlie the development of myocardial ischemia and other mental stress-induced adverse cardiac events in patients with CAD. This study examined for gender-related differences in peripheral arterial response to mental stress in a cohort of patients with CAD using a novel peripheral arterial tonometric (PAT) technique. There were 211 patients (77 women; 37%) with a documented history of CAD and a mean age of 64 +/- 9 years. Patients were enrolled from August 18, 2004, to February 21, 2007. Mental stress was induced using a public speaking task. Hemodynamic and PAT measurements were recorded during rest and mental stress. The PAT response was calculated as a ratio of pulse wave amplitude during stress to at rest. PAT responses were compared between men and women. The PAT ratio (during stress to at rest) was significantly higher in women compared with men. Mean PAT ratio was 0.80 +/- 0.72 in women compared with 0.59 +/- 0.48 in men (p = 0.032). This finding remained significant after controlling for possible confounding factors (p = 0.037). In conclusion, peripheral vasoconstrictive response to mental stress was more pronounced in men compared with women. This finding may suggest that men have higher susceptibility to mental stress-related adverse effects. Additional studies are needed to determine the significance of this finding.

Variability of myocardial ischemic responses to mental versus exercise or adenosine stress in patients with coronary artery disease

Mental stress precipitates myocardial ischemia in a significant percentage of coronary artery disease (CAD) patients. Exercise or adenosine stresses produce different physiologic responses and cause myocardial ischemia via different mechanisms. Little is known about the comparative severity and location of myocardial ischemia provoked by these different stressors. In this study we sought to compare the within-individual ischemic responses to mental versus exercise or adenosine stress in a cohort of CAD patients. All patients underwent mental stress and either exercise or adenosine testing within a 1-week period. Mental stress was induced via a public speaking task. Rest-stress myocardial perfusion imaging was used with all testing protocols. Participants were 187 patients (65 women [35%]) with a documented history of CAD and a mean age of 64 +/- 9 years. Mental stress-induced myocardial ischemia (MSIMI) was less prevalent and frequently of less magnitude than exercise- or adenosine-induced ischemia. Ischemia induced by exercise or adenosine testing did not accurately predict the development or the location of MSIMI. The overall concordance between these stressors for provoking ischemia was weak (percent agreement, 71%; kappa [+/- SE], 0.26 +/- 0.07). In a minority of patients (11%) mental stress provoked ischemia in the absence of exercise- or adenosine-induced ischemia. Moreover, in patients who had myocardial ischemia during both stressors, there were significant within-individual differences in the coronary artery distribution of the ischemic regions. MSIMI was more likely to occur in a single-vessel distribution (86%) compared with exercise- or adenosine-induced ischemia (54%). The stressors had moderate agreement if the ischemic region was in the right coronary artery territory (percent agreement, 76%; kappa, 0.52 +/- 0.19) or the left anterior descending coronary artery (percent agreement, 76%; kappa, 0.51 +/- 0.19) and significantly lower agreement in the left circumflex territory (percent agreement, 62%; kappa, 0.22 +/- 0.18). Our findings indicate that mental and exercise or adenosine stresses provoke different myocardial ischemic responses. These observations suggest that exercise or adenosine testing may not adequately assess the likelihood of occurrence or severity of MSIMI and that different mechanisms are operative in each condition.

Mental stress–induced myocardial ischemia in coronary artery disease patients with left ventricular dysfunction

Reduced left ventricular ejection fraction (LVEF) is a risk factor for poor outcomes in patients with coronary artery disease (CAD). Mental stress-induced myocardial ischemia (MSIMI) also identifies a subset of CAD patients at increased risk for future cardiovascular events. Susceptibility to MSIMI in patients with CAD and reduced LVEF is unknown. We enrolled 182 patients (67 women) with a mean age of 64 years and a documented history of CAD in this study. Baseline resting ejection fraction was determined by use of technetium 99m sestamibi gated single photon emission computed tomography. Abnormal LVEF was defined as less than 45% for men and less than 50% for women (based on published norms for our software [Cedars-Sinai Medical Center]). All participants underwent mental stress testing with a public speaking task. Rest/stress myocardial perfusion single photon emission computed tomography was performed via conventional methodology. Images were visually compared for number and severity of perfusion defects by use of a scoring method from 0 to 4. A summed difference score was calculated as the difference between summed stress and rest scores. A score of greater than 3 was considered abnormal. MSIMI developed in 19% of patients with normal LVEF and 31% of those with reduced LVEF. There is no statistically significant difference between the two groups (P = .11). CAD patients with left ventricular dysfunction are equally susceptible to MSIMI as those with normal LVEF.

Mental Stress Provokes Ischemia in Coronary Artery Disease Subjects Without Exercise- or Adenosine-Induced Ischemia

The purpose of this study was to investigate the possibility that some patients with coronary artery disease (CAD) but negative exercise or chemical stress test results might have mental stress-induced ischemia. The study population consisted solely of those with negative test results. Mental stress-induced ischemia has been reported in 20% to 70% of CAD subjects with exercise-induced ischemia. Because mechanisms of exercise and mental stress-induced ischemia may differ, we studied whether mental stress would produce ischemia in a proportion of subjects with CAD who have no inducible ischemia with exercise or pharmacologic tests. Twenty-one subjects (14 men, 7 women) with a mean age of 67 years and with a documented history of CAD were studied. All subjects had a recent negative nuclear stress test result (exercise or chemical). Subjects completed a speaking task involving role playing a difficult interpersonal situation. A total of 30 mCi 99mTc-sestamibi was injected at one minute into the speech, and imaging was started 40 min later. A resting image obtained within one week was compared with the stress image. Images were analyzed for number and severity of perfusion defects. The summed difference score based on the difference between summed stress and rest scores was calculated. Severity was assessed using a semiquantitative scoring method from zero to four. Six of 21 (29%) subjects demonstrated reversible ischemia (summed difference score > or =3) with mental stress. No subject had chest pain or electrocardiographic changes during the stressor. Mean systolic and diastolic blood pressure and heart rate all increased between resting and times of peak stress. Mental stress may produce ischemia in some subjects with CAD and negative exercise or chemical nuclear stress test results.

Gemfibrozil reduced the risk for coronary events in men with coronary artery disease and low levels of high density lipoprotein cholesterol

(1999) N Engl J Med 341, 410. Rubins HB, Robins SJ, Collins D, et al, . for the Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group. . Gemfibrozil for...

Panic disorder in coronary artery disease patients with noncardiac chest pain

In this study we address the following questions: (1) What percentage of coronary artery disease (CAD) patients that present with chest pain, but whose symptoms cannot be fully explained by their cardiac status, suffer from panic disorder (PD)? (2) How do patients with both CAD and PD compare to patients without CAD and to patients without either PD or CAD in terms of psychological distress? Four hundred forty-one consecutive walk-in emergency department patients with chest pain underwent a structured psychiatric interview (ADIS-R) and completed psychological scales. Fifty-seven percent (250 of 441) of these patients were diagnosed as having noncardiac chest pain and constituted this study's sample. A total of 30% (74 of 250) of noncardiac chest pain patients had a documented history of CAD. Thirty-four percent (25 of 74) of CAD patients met criteria for PD. Patients with both PD and CAD displayed significantly more psychological distress than CAD patients without PD and patients with neither CAD nor PD. However, they did not differ from non-CAD patients with PD. PD is highly prevalent in patients with CAD that are discharged with noncardiac diagnoses. The psychological distress in these patients appears to be related to the panic syndrome and not to the presence of the cardiac condition.

973-112 Prognostic Value of TroponinT, Myoglobin and CK-MB Mass in Patients with Chest Pain without Acute Myocardial Infarction

We investigated the prognostic value of Minimal Myocardial Damage (MMD) as indicated by minor elevations of TroponinT (TnT), Myoglobin (Myo) and CK-MB Mass (CK-MB) in 128 patients (pts) presented with chest pain at the emergency room (ER) in whom an acute myocardial infarction (AMI) was excluded. Blood was drawn 3, 4, 5, 6, 7, 8, 12, 16, 20, 24 hours after the onset of symptoms. Gold standard for AMI was a typical rise and fall of the CK-MB curve with a peak&gt; 14 ng/ml. A minor elevation of CK-MB was considered present if the marker showed a typical rise and fall but with a peak below 14 ng/ml. TnT was considered abnormal if it showed a gradual rise with a highest value &gt;0.01 ng/ml, Myo was considered abnormal if tie curve showed a typical rise and fall with highest value at least tvvice the lowest value. Only CK-MB results were reported to the attending physician. A documented history of Coronary Artery Disease (CAD) was defined as either previous AMI, PTCA, CABG or a previous positive exercise test. Pts with unstable angina were admitted to the CCU and stabilized with intravenous nitrates, aspirin, heparin, β-blockers and Calcium-antagonists. PTCA or CABG was performed for recurrent refractory angina. Follow up was completed after six months. Major events were cardiac death and AMI, minor events were PTCA and CABG. Diagnosis was unstable angina in 54 pts, stable angina in 59 pts, atypical chest pain in 13 pts and arrhythmia in 2 pts. 75 Pts had a documented history of CAD. MMD was indicated by abnormal TnT in 24 pts, by CK-MB in 13 pts and by Myo in 20 pts. There were 24 events (3 major and 21 minor). 20 events occurred in pts with a history of CAD (Relative Risk: RR, 95% Confidence Limits CL: 3.53, 1.28–9.74). Events rate for TnT was 8/24 (RR: 2.17, 95% CL: 1.05–4.47), CK-MB 4/13 (RR: 1.77, 95% CL: 0.71–4.38) and Myo 5/20 (RR: 1.42, 95%CL: 0.60–3.361 Minor elevations of CK-MB or Myoglobin have limited prognostic value in pts presented at the ER with chest pain in whom an AMI has been excluded. Minor elevation of TnT has some prognostic value but the best predictor of future events in this group is a history of CAD.