2016 Vol. 13, No. 2
Coronary heart disease remains the leading cause of death in the developed world. Advanced age is the single strongest risk factor for coronary artery disease (CAD) and independent predictor for poor outcomes following an acute coronary syndrome (ACS). ACS refers to a spectrum of conditions compatible with acute myocardial ischemia and/or infarction due to various degrees of reduction in coronary blood flow as a result of plaque rupture/erosion and thrombosis formation or supply and demand mismatch. Unstable angina and non -ST segment elevation myocardial infarction are often continuous and clinically indistinguishable, collectively referred as non -ST elevation ACS (NSTE-ACS). An abrupt total occlusion of a coronary artery causing transmural myocardial ischemia/necrosis and displaying ST segment elevation or new left bundle branch block on a12-lead electrocardiogram (ECG) leads to the diagnosis of ST segment elevation myocardial infarction (STEMI). NSTE-ACS and STEMI require acute cardiac care. Professional societies have established guidelines for high quality contemporary care for ACS patients, i.e. American Heart Association/American College of Cardiology guidelines for STEMI1 andNSTE-ACS2, European Society of Cardiology guidelines for STEMI3 and NSTE-ACS4, and the United Kingdom National Institute for Health and Care Excellence (NICE) guidelines for STEMI5 and NSTE-ACS.6 Implementation of evidence-based therapies has significantly decreased mortality and morbidities of ACS.3, 7, 8 However, these advancements in ACS management have not equally improved outcomes for older adults. Vulnerable older patients continue to be at high risk of poor outcomes, are less likely to receive evidence based care, and have high mortality rates regardless of treatments given.9, 10 These disparities and challenges in caring for ACS in older adults are well recognized.11-13 This review summarizes the increasing burden and persistent unfavorable outcome of ACS in older adults, and discusses the clinical presentation, diagnosis and strategies for medical and invasive therapy.
Ischemic heart disease (IHD) is caused by atherosclerotic and/or thrombotic obstruction of coronary arteries. Clinical spectrum of IHD expands from asymptomatic atherosclerosis of coronary arteries to acute coronary syndromes (ACS) including unstable angina, acute myocardial infarction (non-ST elevation myocardial infarction and ST elevation myocardial infarction). Stable IHD (SIHD) refers to patients with known or suspected IHD who have no recent or acute changes in their symptomatic status, suggesting no active thrombotic process is underway. These patients include those with i) recent-onset or stable angina or ischemic equivalent symptoms, such as dyspnea or arm pain with exertion; ii) post-ACS stabilized after revascularization or medical therapy; and iii) asymptomatic IHD diagnosed by abnormal stress tests or imaging studies. This review summarizes clinical features and management of SIHD in the older adult. ACS in older adults is not considered in this review.
Cardiac resynchronization therapy (CRT) is associated with a favorable outcome only in patients with left bundle branch block (LBBB) pattern and in patients with a QRS duration > 150 ms, in patients with non-LBBB pattern with a QRS duration of 120–150 ms usually is not beneficial. After adjusting for QRS duration, QRS morphology was no longer a determinant of the clinical response to CRT. In contrast to the mainstream view, we hypothesized that the unfavorable CRT outcome in patients with non-LBBB and a QRS duration of 120–150 ms is not due to the QRS morphology itself, but to less dyssynchrony and unfavorable patient characteristics in this subgroup, such as more ischemic etiology and greater prevalence of male patients compared with patients with LBBB pattern. Further, the current CRT technique is devised to eliminate the dyssynchrony present in patients with LBBB pattern and inappropriate to eliminate the dyssynchrony in patients with non-LBBB pattern. We also hypothesized that electrocardiography may also provide information about the presence of interventricular and left intraventricular dyssynchrony and the approximate location of the latest activated left ventricular (LV) region. To this end, we devised new ECG criteria to estimate interventricular and LV intraventricular dyssynchrony and the approximate location of the latest activated LV region. Our preliminary data demonstrated that the latest activated LV region in patients with nonspecific intraventricular conduction disturbance (NICD) pattern might be at a remote site from that present in patients with LBBB pattern, which might necessitate the invention of a novel CRT technique for patients with NICD pattern. The application of the new interventricular and LV intraventricular dyssynchrony ECG criteria and a potential novel CRT technique might decrease the currently high nonresponder rate in patients with NICD pattern.
Objective To assess the influence of age on the error of estimate (EE) of maximal oxygen uptake (VO2max) using sex and population specific-equations in cycle ergometer exercise testing, since estimated VO2max is associated with a substantial EE, often exceeding 20%, possibly due to intrinsic variability of mechanical efficiency. Methods 1850 adults (68% men), aged 18 to 91 years, underwent maximal cycle ergometer cardiopulmonary exercise testing. Cardiorespiratory fitness (CRF) was assessed relative to sex and age [younger (18 to 35 years), middle-aged (36 to 60 years) and older (> 60 years)]. VO2max [mL?(kg?min)?1] was directly measured by assessment of gas exchange and estimated using sex and population specific-equations. Measured and estimated values of VO2max and related EE were compared among the three age- and sex-specific groups. Results Directly measured VO2max of men and women were 29.5 ± 10.5 mL?(kg?min)?1 and 24.2 ± 9.0 mL?(kg?min)?1 (P ?1] and percent errors (%E) for men and women had similar values, 0.5 ± 3.2 and 0.4 ± 2.9 mL?(kg?min)?1, and ?0.8 ± 13.1% and ?1.7 ± 15.4% (P > 0.05), respectively. EE and %E for each age-group were, respectively, for men: younger = 1.9 ± 4.1 mL?(kg?min)?1 and 3.8 ± 10.5%, middle-aged = 0.6 ± 3.1 mL?(kg?min)?1 and 0.4 ± 10.3%, older = ?0.2 ± 2.7 mL?(kg?min) ?1 and ?4.2 ± 16.6% (P ?1 and 2.7 ± 10.0%, middle-aged = 0.7 ± 2.8 mL?(kg?min)?1 and 0.5 ± 11.1%, older = -0.8 ± 2.3 mL?(kg?min)?1 and ?9.5 ± 22.4% (P Conclusion VO2max were underestimated in younger age-groups and were overestimated in older age groups. Age significantly influences the magnitude of the EE of VO2max in both men and women and should be considered when CRF is estimated using population specific equations, rather than directly measured.
Background Although particulate matter, with diameters 2.5) and 10), and other pollutants have been associated with cardiovascular morbidity and mortality, the effect of pollutants on acute myocardial infarctions (AMIs) has rarely been investigated in Asia, especially in Shanghai, China. Methods Between 1 November 2013 and 27 April 2014, 972 patients from the Pudong District, Shanghai City, were assessed by the Emergency Medical Service. A case-crossover design was used to analyze exposure to air pollution and the AMI risk. Exposures to PM2.5, PM10, nitrogen dioxide (NO2), sulphurdioxide (SO2), and carbon monoxide (CO) were based on the mean urban background levels. The associations among AMI admissions, the included pollutants, temperature, and relative humidity were analyzed using correlation and logistic regression. Results The urban background levels of PM2.5, PM10 and CO were associated with an increased risk of AMI, unlike NO2 and SO2 levels. The OR (95% CI) for AMI were 1.16 (1.03–1.29), 1.05 (1.01–1.16), 0.82 (0.75–1.02), 0.87 (0.63–1.95), and 1.08 (1.02-1.21) for PM2.5, PM10, NO2, SO2, and CO, respectively. Increases in the air quality index (AQI) were associated with more AMI occurrences. There was no correlation between fluctuations in temperature and relative humidity with AMI hospital admissions. Conclusions Short-term exposure to moderate-serious pollution levels is associated with increased risk of AMI. Increased PM2.5, PM10 and CO levels are related to increased AMI admissions.
Objectives To study the association of single nucleotide polymorphism (SNP) rs2076185 in chromosome 6p24.1 with the premature coronary artery diseases (PCAD) in Chinese Han population. Methods A total of 1382 patients were divided into the PCAD group and the control group based on their coronary arteriography (CAG) results. Their SNP rs2076185 were analyzed by the mass-spectrometry. Their allele and genotype frequency in Hardy-Weinberg equilibrium were calculated for assessment. Logistic regression was employed to remove confounding factors and correlate SNP rs2076185 with PCAD. Results The allele and genotype frequencies of the control group were in Hardy-Weinberg equilibrium (P > 0.05). The frequencies of allele G of rs2076185 were 54.2% in the PCAD group and 49.5% in the control group. The difference was significant (P = 0.042). The genotype distribution of rs2076185 of the two groups was also significantly different. The univariate analysis showed that the rs2076185 polymorphisms were associated with the PCAD only in the additive model (OR: 0.828, 95% CI: 0.711?0.964, P = 0.014), and in the dominant model (OR: 0.753, 95% CI: 0.591?0.958, P = 0.021). After removing the confounding variables, the rs2076185 polymorphisms was associated with PCAD in the additive model (OR: 0.775, 95% CI: 0.648?0.928, P = 0.005), in the dominant model (OR: 0.698, 95% CI: 0.527?0.925, P = 0.012), and in the recessive model (OR: 0.804, 95% CI: 0.538?0.983, P = 0.038). Conclusion Allele G of rs2076185 reduces the PCAD risks in Chinese Han population, therefore it could be a coronary artery diseases protective factor in Chinese Han population.
Objective To investigate whether coronary artery revascularization therapies (CART), including percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG), can improve the in-hospital and long-term outcomes for acute myocardial infarction (AMI) patients with prior ischemic stroke (IS). Methods A total of 387 AMI patients with prior IS were enrolled consecutively from January 15, 2005 to December 24, 2011 in this cohort study. All patients were categorized into the CART group (n = 204) or the conservative medications (CM) group (n = 183). In-hospital cardiocerebral events and long-term mortality of the two groups after an average follow-up of 36 months were recorded by Kaplan-Meier survival curves and compared by Logistic regression and the Cox regression model. Results The CART patients were younger (66.5 ± 9.7 years vs. 71.7 ± 9.7 years, P P = 0.016) and more multiple-vascular coronary lesions (50% vs. 69.4%, P = 0.031). The hospitalization incidence of cardiocerebral events in the CART group was 9.3% while 26.2% in the CM group (P n = 137) and 24 cases (12.2%) died in CART group (n = 197). Cox regression indicated that CART decreased the long-term mortality by 72% [adjusted hazard ratio (HR) = 0.28, 95% CI: 0.06–0.46], while categorical analysis indicated no significant difference between PCI and CABG. Conclusions CART has a significant effect on improving the in-hospital and long-term prognoses for AMI patients with prior IS.
Background Many studies have indicated that medical therapy and percutaneous coronary intervention have similar effects in terms of the long-term prognosis of patients with stable coronary artery disease. This study investigated the effects of optimal medical therapy (OMT) and revascularization-plus-OMT in elderly patients with high-risk angina. Methods In this prospective non-randomized study, 241 consecutive high-risk elderly male patients (65–92 years of age) with angiographically confirmed multivessel disease were enrolled in the registry from January 2004 to April 2005. Of these, 98 patients underwent OMT and 143 underwent revascularization therapy plus OMT. Results After 6.5 years of follow-up, we found that the rate of long-term cardiac mortality was significantly higher in patients who underwent OMT than in those who underwent revascularization (6.5-year unadjusted mortality rate, 14.3% for OMT vs. 7.0% for revascularization patients; log-rank P = 0.04). However, the overall risks of major adverse cardiac cerebrovascular events (MACCE) were similar among all patients (6.5-year unadjusted mortality rate, 29.6% for OMT vs. 27.3% for revascularization patients; log-rank P = 0.67). Conclusions OMT was associated with an increase in cardiac death but a similar 6.5-year risk of MACCE compared with revascularization in high-risk elderly male patients with coronary multivessel disease.
Background Thalassemic patients demonstrate an increased rate of extracardiac vascular complications and increased carotid wall intima-media thickness (cIMT), but very low prevalence of coronary artery disease (CAD). We investigated the atheroma burden by assessing the coronary artery calcium (CAC) and cIMT in these patients. Methods We examined 37 patients with β-thalassemia and 150 healthy control volunteers with multi-detector computer tomography (CT) and ultrasonography to determine CAC score and cIMT, respectively. Results Propensity score matching (C-statistic: 0.88; 95% CI: 0.83–0.93) resulted in 27 pairs of patients; severe CAC was observed in 2 (7.4%) and 0 of β-thalassemia patients and healthy volunteers respectively (P = 0.5). Median calcium score was 0 (0–0) in β-thalassemia patients and 0 (0–4) in healthy volunteers (P = 0.8). Median intima-media thickness was higher in β-thalassemia patients compared to control group [0.45 (0.06–0.65) vs. 0.062 (0.054–0.086); P = 0.04]. Conclusions Patients with β–thalassemia in comparison with healthy control subjects exhibit similar CAC score and increased cIMT. Our findings indicate a disparate rate of progression of atherosclerosis between coronary and extracardiac arteries in these patients lending support to the epidemiological evidence.
Background Pulmonary veins (PV) and the atria undergo electrical and structural remodeling in atrial fibrillation (AF). This study aimed to determine PV and left atrial (LA) reverse remodeling after catheter ablation for AF assessed by chest computed tomography (CT). Methods PV electrophysiologic studies and catheter ablation were performed in 63 patients (68% male; mean ± SD age: 56 ± 10 years) with symptomatic AF (49% paroxysmal, 51% persistent). Chest CT was performed before and 3 months after catheter ablation. Results At baseline, patients with persistent AF had a greater LA volume (91 ± 29 cm3 vs. 66 ± 27 cm3; P = 0.003) and mean PV ostial area (241 ± 43 mm2 vs. 212 ± 47 mm2; P = 0.03) than patients with paroxysmal AF. There was no significant correlation between the effective refractory period and the area of the left superior PV ostium. At 3 months of follow-up after ablation, 48 patients (76%) were AF free on or off antiar?rhythmic drugs. There was a significant reduction in LA volume (77 ± 31 cm3 to 70 ± 28 cm3; P 2 to 182 ± 43 mm2; P 3 vs. 4.0 ± 11.2 cm3; P = 0.04) and PV ostial area (62 mm2 vs. 34 mm2; P = 0.04) than those who have paroxysmal AF. The reduction of the averaged PV ostial area was significantly correlated with the reduction of LA volume (r = 0.38, P = 0.03). Conclusions Catheter ablation of AF improves structural remodeling of PV ostia and left atrium. This finding is more apparent in patients with persistent AF treated by catheter ablation.
Objective To identify clinical characteristics associated with the minimum lumen area (MLA) of proximal or middle intermediate lesions in the left anterior descending (LAD) artery, and to develop a model to predict MLA. Methods We retrospectively analyzed demographic data, medical history, and intravascular ultrasound findings for 90 patients with intermediate lesions in the LAD artery. Linear regression was used to identify factors affecting MLA, and multiple regression was used to develop a model for predicting MLA. Results Age, number of lesions, and diabetes mellitus correlated significantly with MLA of proximal or middle intermediate lesions. A regression model for predicting MLA (mm2) was derived from the data: 7.00 ? 0.05 × (age) ? 0.50 × (number of lesions). A cut-off value of 3.1 mm2 was proposed for deciding when to perform percutaneous coronary intervention. Conclusion This model for predicting MLA of proximal or middle intermediate lesions in the LAD artery showed high accuracy, sensitivity, and specificity, indicating good diagnostic potential.
Thiazide-induced hyponatremia is one of the main causes of decreased sodium levels in elderly individuals. This review presents the current evidence regarding the thiazide-associated hyponatremia. Thiazide-associated hyponatremia is observed mainly in patients with certain risk factors such as those receiving large doses of thiazides, having much comorbidity, such as heart failure, liver disease or malig-nancy, and taking several medications, such as non-steroidal anti-inflammatory drugs, selective serotonin re-uptake inhibitors or tricyclic antidepressants. Sodium concentration should be monitored in patients with risk factors for developing thiazide-associated hyponatremia and clinicians should measure promptly serum sodium levels in patients with neurologic signs indicating reduced sodium levels. The clini-cal and biochemical profile of patients with thiazide-associated hyponatremia may be that of extracellular volume depletion or the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The investigation of possible thiazide-associated hyponatremia includes the exclusion of other causes of decreased sodium levels and the identification of the characteristics of hyponatremia due to thiazides (ex-tracellular volume depletion-related or SIADH-like). Treatment should be carefully monitored to avoid serious neurologic complications due to overcorrection. Clinicians should discourage prescribing thiazides in patients with a history of diuretic-associated hyponatremia and should prefer low doses of thiazides in patients with risk factors for developing thiazide-associated hyponatremia.
The roles of androgens on cardiovascular physiology and pathophysiology are controversial as both beneficial and detrimental effects have been reported. Although the reasons for this discrepancy are unclear, multiple factors such as genetic and epigenetic variation, sex-specificity, hormone interactions, drug preparation and route of administration may contribute. Recently, growing evidence suggests that androgens exhibit beneficial effects on cardiovascular function though the mechanism remains to be elucidated. Endothelial cells (ECs) which line the interior surface of blood vessels are distributed throughout the circulatory system, and play a crucial role in cardiovascular function. Endothelial progenitor cells (EPCs) are considered an indispensable element for the reconstitution and maintenance of an intact endothelial layer. Endothelial dysfunction is regarded as an initiating step in development of atherosclerosis and cardiovascular diseases. The modulation of endothelial functions by androgens through either genomic or nongenomic signal pathways is one possible mechanism by which androgens act on the cardiovascular system. Obtaining insight into the mechanisms by which androgens affect EC and EPC functions will allow us to determine whether androgens possess beneficial effects on the cardiovascular system. This in turn may be critical in the prevention and therapy of cardiovascular diseases. This article seeks to review recent progress in androgen regulation of endothelial function, the sex-specificity of androgen actions, and its clinical applications in the cardiovascular system.