Atrial fibrillation incidence after coronary artery bypass graft surgery and percutaneous coronary intervention: the prospective AFAF cohort study.

Objectives. Atrial fibrillation is a common arrhythmia in patients with ischemic heart disease. This study aimed to determine the cumulative incidence of new-onset atrial fibrillation after percutaneous coronary intervention or coronary artery bypass grafting surgery during 30 days of follow-up. Design. This was a prospective multi-center cohort study on atrial fibrillation incidence following percutaneous coronary intervention or coronary artery bypass grafting for stable angina or non-ST-elevation acute coronary syndrome. Heart rhythm was monitored for 30 days postoperatively by in-hospital telemetry and handheld thumb ECG recordings after discharge were performed. The primary endpoint was the cumulative incidence of atrial fibrillation 30 days after the index procedure. Results. In-hospital atrial fibrillation occurred in 60/123 (49%) coronary artery bypass graft and 0/123 percutaneous coronary intervention patients (p < .001). The cumulative incidence of atrial fibrillation after 30 days was 56% (69/123) of patients undergoing coronary artery bypass grafting and 2% (3/123) of patients undergoing percutaneous coronary intervention (p < .001). CABG was a strong predictor for atrial fibrillation compared to PCI (OR 80.2, 95% CI 18.1-354.9, p < .001). Thromboembolic stroke occurred in-hospital in one coronary artery bypass graft patient unrelated to atrial fibrillation, and at 30 days in two additional patients, one in each group. There was no mortality. Conclusion. New-onset atrial fibrillation during 30 days of follow-up was rare after percutaneous coronary intervention but common after coronary artery bypass grafting. A prolonged uninterrupted heart rhythm monitoring strategy identified additional patients in both groups with new-onset atrial fibrillation after discharge.

Coronary computed tomography angiography derived fractional flow reserve and risk of recurrent angina: A 3-year follow-up study.

BACKGROUND: The association between coronary computed tomography angiography (CTA) derived fractional flow reserve (FFRCT) and risk of recurrent angina in patients with new onset stable angina pectoris (SAP) and stenosis by CTA is uncertain. METHODS: Multicenter 3-year follow-up study of patients presenting with symptoms suggestive of new onset SAP who underwent first-line CTA evaluation and subsequent standard-of-care treatment. All patients had at least one ≥30 â€‹% coronary stenosis. A per-patient lowest FFRCT-value ≤0.80 represented an abnormal test result. Patients with FFRCT ≤0.80 who underwent revascularization were categorized according to completeness of revascularization: 1) Completely revascularized (CR-FFRCT), all vessels with FFRCT ≤0.80 revascularized; or 2) incompletely revascularized (IR-FFRCT) ≥1 vessels with FFRCT ≤0.80 non-revascularized. Recurrent angina was evaluated using the Seattle Angina Questionnaire. RESULTS: Amongst 769 patients (619 [80 â€‹%] stenosis ≥50 â€‹%, 510 [66 â€‹%] FFRCT ≤0.80), 174 (23 â€‹%) reported recurrent angina at follow-up. An FFRCT ≤0.80 vs â€‹> â€‹0.80 associated to increased risk of recurrent angina, relative risk (RR): 1.82; 95 â€‹% CI: 1.31-2.52, p â€‹< â€‹0.001. Risk of recurrent angina in CR-FFRCT (n â€‹= â€‹135) was similar to patients with FFRCT >0.80, 13 â€‹% vs 15 â€‹%, RR: 0.93; 95 â€‹% CI: 0.62-1.40, p â€‹= â€‹0.72, while IR-FFRCT (n â€‹= â€‹90) and non-revascularized patients with FFRCT ≤0.80 (n â€‹= â€‹285) had increased risk, 37 â€‹% vs 15 â€‹% RR: 2.50; 95 â€‹% CI: 1.68-3.73, p â€‹< â€‹0.001 and 30 â€‹% vs 15 â€‹%, RR: 2.03; 95 â€‹% CI: 1.44-2.87, p â€‹< â€‹0.001, respectively. Use of antianginal medication was similar across study groups. CONCLUSION: In patients with SAP and coronary stenosis by CTA undergoing standard-of-care guided treatment, FFRCT provides information regarding risk of recurrent angina.

Patients with Moderate Non-Culprit Coronary Lesions of Recent Acute Coronary Syndrome.

Fractional flow reserve (FFR) measurement was compared to dobutamine stress echocardiography (DSE) instable angina (SA) with stable coronary lesion (s) (SCL (s) ) in a few trials; however, similar comparisons in patients with acute coronary syndrome (ACS) with non-culprit lesion (s) (NCL (s) ) are lacking. Our objectives were to prospectively evaluate the diagnostic performance of FFR with two different cutoff values (< 0.80 and < 0.75) relative to DSE in moderate (30%-70% diameter stenosis) NCLs (ACS group) and to compare these observations with those measured in SCLs (SA group). One hundred seventy-five consecutive patients with SA (n = 86) and ACS (n = 89) with 225 coronary lesions (109 SCLs and 116 NCLs) were enrolled. In contrast to the ACS cohort in SA patients, normal DSE was associated with higher FFR values compared to those with abnormal DSE (P = 0.051 versus P = 0.006). In addition, in the SA group, a significant correlation was observed between DSE (regional wall motion score index at peak stress) and FFR (r = -0.290; P = 0.002), whereas a similar association was absent (r = -0.029; P = 0.760) among ACS patients. In the SA group, decreasing the FFR cutoff value (< 0.80 versus < 0.75) improved the concordance of FFR with DSE (70.6% versus 81.7%) without altering its discriminatory power (area under the curve; 0.68 versus 0.63; P = 0.369), whereas in the ACS group, concordance remained similar (69.0% versus 71.6%) and discriminatory power decreased (0.62 versus 0.51; P = 0.049), respectively. In conclusion, lesion-specific FFR assessment may have different relevance in patients with moderate NCLs than in patients with SCLs.

Decreased continuous sitting time increases heart rate variability in patients with cardiovascular risk factors.

AIM: The purpose of the present study was to elucidate the relationship between high-frequency heart rate variability (HF HRV) and continuous daytime sitting time in patients with cardiovascular risk factors such as mild hypertension and/or stable angina pectoris. BACKGROUND: Decreased HF HRV precedes the progression and worsening of cardiovascular diseases. Continuous sitting behavior is a major risk factor for developing metabolic syndrome and is associated with cardiovascular disease, diabetes mellitus, renal failure, sarcopenia and osteoporosis. Risk factors for cardiovascular disease can be affected by continuous daytime sitting behaviors. DESIGN: The present study design was a post-hoc comparison. METHODS: Patients treated at two different primary care clinics from 2014 to 2018 were enrolled in this study (n = 53). We assessed HF HRV and continuous sitting time using 24-hour Holter electrocardiography and an activity meter at baseline and 6 months. HF HRV was calculated during sleep. RESULTS: Sitting time had decreased in 22 patients (decreased group) and increased in 31 patients (increased group) after 6 months. The mean patient ages were 73.1 and 72.0 years in the decreased and increased sitting time groups, respectively (p = 0.503). HF HRV during sleep had increased after 6 months in the decreased sitting time group. Compared with the increased group, the decreased group showed significantly higher HF HRV during sleep after 6 months by two-way repeated-measures ANOVA after adjustment for age, sex and change in activity (p = 0.045). CONCLUSION: These results suggest that a decrease in sitting time might induce parasympathetic activity during sleep. Therefore, reducing continuous sitting time during the day might contribute, in part, to improving the prognosis of patients with cardiovascular risk factors not only by avoiding muscle loss but also by providing positive influences on parasympathetic tone during sleep.

Relation of renal function to mid-term prognosis of stable angina patients with high- or low-dose pitavastatin treatment: REAL-CAD substudy.

BACKGROUND: It has not yet been established whether higher-dose statins have beneficial effects on cardiovascular events in patients with stable coronary artery disease (CAD) and renal dysfunction. METHODS: The REAL-CAD study is a prospective, multicenter, open-label trial. As a substudy, we categorized patients by an estimated glomerular filtration rate (eGFR) as follows: eGFR ≥60 (n = 7,768); eGFR ≥45 and <60 (n = 3,176); and eGFR <45 mL/Min/1.73 m2 (n = 1,164), who were randomized to pitavastatin 4mg or 1mg therapy. The primary endpoint was a composite of cardiovascular death, non-fatal myocardial infarction, non-fatal ischemic stroke, or unstable angina, and was assessed by the log-rank test and Cox proportional hazards model. RESULTS: The baseline characteristics and medications were largely well-balanced between two groups. The magnitude of low-density lipoprotein cholesterol (LDL-C) reduction at 6 months in high- and low-dose pitavastatin groups was comparable among all eGFR categories. During a median follow-up of 3.9 years, high- compared with low-dose pitavastatin significantly reduced cardiovascular events in patients with eGFR ≥60 (hazard ratio (HR) 0.73; 95% confidence interval (CI) 0.58-0.91; P = .006), and reduced but not significant for patients with eGFR ≥45 and <60 (HR 0.85; 95% CI, 0.63-1.14; P = .27) or eGFR <45 mL/Min/1.73 m2 (HR 0.90; 95% CI 0.62-1.33; P = .61). An interaction test of treatment by eGFR category was not significant (P value for interaction = .30). CONCLUSION: Higher-dose pitavastatin therapy reduced LDL levels and cardiovascular events in stable CAD patients irrespective of eGFR level, although the effect on events appeared to be numerically lower in patients with lower eGFR.

Elevated plasma fatty acid-binding protein 3 is related to prolonged corrected QT interval and reduced ejection fraction in patients with stable angina.

Background: Higher concentrations of plasma fatty acid-binding protein 3 (FABP3) play a role in the development of cardiovascular events, cerebrovascular deaths, and acute heart failure. However, little is known about the relationship between plasma FABP3 level and prolonged QT interval and reduced ejection fraction (EF). This study aimed to investigate the relationship between plasma FABP3 level and prolonged corrected QT (QTc) interval and reduced EF in patients with stable angina. Inflammatory cytokine and adipocytokine levels were also measured to investigate their associations with plasma FABP3. Methods: We evaluated 249 consecutive patients with stable angina. Circulating levels of FABP3 were measured by ELISA. In addition, 12-lead ECG and echocardiography recordings were obtained from each patient. Results: Multiple regression analysis showed that high-density lipoprotein cholesterol, high sensitivity C-reactive protein (hs-CRP), white blood cell (WBC) count, visfatin, adiponectin, FABP4, heart rate, QTc interval, left atrial diameter, left ventricular mass index, end-systolic volume, end-systolic volume index, fractional shortening, and EF were independently associated with FABP3 (all p<0.05). Patients with an abnormal QTc interval had a higher median plasma FABP3 level than those with a borderline and normal QTc interval. With increasing FABP3 tertiles, the patients had higher frequencies of abnormal QTc interval, left ventricular systolic dysfunction, and all-cause mortality, incrementally lower EF, higher WBC count, and higher levels of hs-CRP, visfatin, adiponectin, and FABP4. Conclusion: This study indicates that plasma FABP3 may act as a surrogate parameter of prolonged QTc interval and reduced EF in patients with stable angina, partially through the effects of inflammation or cardiomyocyte injury. Further studies are required to elucidate whether plasma FABP3 plays a role in the pathogenesis of QTc prolongation and reduced EF.

Relation of Obstructive Sleep Apnea in Patients With a Coronary Chronic Total Occlusion to Coronary Collaterals and Mortality.

A chronic total occlusion (CTO) is frequently identified in patients undergoing coronary angiography. The prognostic implications of intermittent hypoxia from obstructive sleep apnea (OSA) on patients with a CTO, and effects on collateral recruitment are unknown. The aim of this study was to determine the prevalence, vascular effects, and prognostic implications of the presence of OSA in patients with a CTO. Patients with a CTO between July 2010 and December 2019 were reviewed. Electronic medical records were accessed to determine documented patient history of OSA, demographics, and clinical course. Patients with robust collateral recruitment were defined as Rentrop grade 2 or 3. A total of 948 patients were included in the study, of which 127 (13.4%) had a documented history of OSA. These patients were younger (67.0 years vs 70.6 years, p < 0.01), had a higher body mass index (29.6 kg/m2 vs 26.7 kg/m2, p < 0.0001), higher rates of hypertension (91.3% vs 83.2%, p < 0.05), higher rates of smokers (63.3% vs 49.0%, p < 0.01) and more use of ß-blockers (79% vs 68.5%, p < 0.05) and statins (92.7% vs 82.1%, p < 0.01). A documented history of OSA was independently associated with robust collaterals (OR 3.0 95%CI 1.5 to 5.8, p < 0.01) and lower mortality (HR 0.3 95% CI 0.1 to 0.7, p < 0.01) with a mean survival of 10.8 years, as compared to 8.1 years (log rank p < 0.0001). In conclusion, in patients with a CTO, documented OSA is independently associated with more robust coronary collaterals and lower mortality. The possible cardioprotective implications of intermittent hypoxia in OSA, as well as treatment effect requires further investigation.

Coronary artery lumen complexity as a new marker for refractory symptoms in patients with vasospastic angina.

Refractory angina is an independent predictor of adverse events in patients with vasospastic angina (VSA). The aim of this study was to investigate the relationship between coronary lumen complexity and refractory symptoms in patients with VSA. Seventeen patients with VSA underwent optical coherence tomography. The patients were divided into the refractory VSA group (n = 9) and the stable VSA group (n = 8). A shoreline development index was used to assess the coronary artery lumen complexity. Shear stress was estimated using a computational fluid dynamics model. No difference was observed in the baseline characteristics between the two groups. The refractory VSA group showed the higher shoreline development index (refractory VSA 1.042 [1.017-1.188] vs stable VSA 1.003 [1.006-1.025], p = 0.036), and higher maximum medial thickness (refractory VSA 184 ± 17 µm vs stable VSA 148 ± 31 µm, p = 0.017), and higher maximum shear stress (refractory VSA 14.5 [12.1-18.8] Pa vs stable VSA 5.6 [3.0-10.5] Pa, p = 0.003). The shoreline development index positively correlates with shear stress (R2 = 0.46, P = 0.004). Increased medial thickness of the coronary arteries provokes lumen complexity and high shear stress, which might cause refractory symptoms in patients with VSA. The shoreline index could serve as a marker for irritability of the medial layer of coronary arteries and symptoms.

Comparison of mitral annular displacement and global longitudinal strain imaging for predicting significant coronary atherosclerotic disease in patients of chronic stable angina pectoris.

Myocardial strain by two-dimensional speckle-tracking echocardiography (2D-STE) is a validated clinical index of myocardial deformation, for predicting CAD in patients with chronic stable angina pectoris (CSAP) with preserved ejection fraction (EF). However, it is complex, imaging dependant with intra and intervendor variability. The mitral annulus displacement (MAD) has been correlated to left ventricular (LV) longitudinal deformation and may be interchanged with strain imaging. This cross-sectional study was conducted on patients with suspected CSAP (n = 146) and preserved LVEF without wall motion abnormalities. We excluded patients with prior heart disease, ACS, arrhythmia, heart failure or poor imaging. GLS, Average MAD and normalized MAD were calculated using 2D-STE by automated function imaging. CAG was gold standard. MAD had significantly lesser dropout due to suboptimal imaging. Receiver operating characteristic (ROC) analysis showed that GLS had significantly better area under curve (AUC) compared to Normalised MAD and Average MAD (P = 0.035) in predicting significant CAD in patients of CSAP. The optimal cut-off of GLS, normalized MAD and Average MAD were ≥ - 20.67% (sensitivity 94.2%, specificity 86.7%), ≤ 15.22% (sensitivity 90.7%, specificity 80%) and ≤ 11.18 mm (sensitivity 83.7%, specificity 71.1%) respectively. GLS showed strong correlation with Normalised MAD (R = 0.669, P < 0.001) and good correlation to Average MAD (R 0.572, P < 0.001). Absolute GLS and Normalised MAD showed significant inverse correlation to SYNTAX score. GLS is a more accurate measure for predicting presence and severity of CAD then MAD however latter is a reliable simpler, robust, and expeditious tool with lesser dropouts. It can be at least of complementary value to other imaging markers for myocardial function when LV curvatures are poorly visualized or in busy outdoors with time constraint.

Comparison of functional exercise capacity, quality of life and respiratory and peripheral muscle strength between patients with stable angina and healthy controls.

OBJECTIVE: We aimed to compare functional exercise capacity, respiratory and peripheral muscle strength, pulmonary function and quality of life between patients with stable angina and healthy controls. METHODS: We compared 33 patients with stable angina (55.21 ± 6.12 years old, Canada Class II-III, left ventricular ejection fraction: 61.92 ± 7.55) and 30 healthy controls (52.70 ± 4.22 years old). Functional capacity (6-minute walk test (6-MWT)), respiratory muscle strength (mouth pressure device), peripheral muscle strength (dynamometer), pulmonary function (spirometer) and quality of life (Short Form 36 (SF-36)) were evaluated. RESULTS: 6-MWT distance (499.20 ± 51.91 m versus 633.05 ± 57.62 m), maximal inspiratory pressure (85.42 ± 20.52 cmH2O versus 110.44 ± 32.95 cmH2O), maximal expiratory pressure (83.33 ± 19.05 cmH2O versus 147.96 ± 54.80 cmH2O) and peripheral muscle strength, pulmonary function and SF-36 sub-scores were lower in the angina group versus the healthy controls, respectively. CONCLUSION: Impaired peripheral and respiratory muscle strength, reduction in exercise capacity and quality of life are obvious in patients with stable angina. Therefore, these parameters should be considered in stable angina physiotherapy programmes to improve impairments.

High fructose consumption may be associated with slow coronary flow.

OBJECTIVE: The precise pathophysiology of slow coronary flow (SCF) has not yet been clarified; however, many studies have shown that significant fructose consumption is associated with oxidative stress and inflammation, which may play a role in the pathophysiology of SCF. The aim of this study was to investigate the association between fructose consumption and isolated SCF. METHODS: Patients with stable angina pectoris who underwent coronary angiography between December 2018 and April 2019 were evaluated for this study. In all, 45 patients with isolated SCF were selected as the patient group (SCF group) and 50 patients with a normal coronary flow pattern were enrolled as a control group. Participants used a dietary record to provide details of nutrient consumption and all of the data from the 2 groups were compared. RESULTS: The high-sensitivity C-reactive protein (Hs-CRP) level (p=0.024), white blood cell count (p=0.038), and smoking rate (p=0.012) were higher in the SCF group. Total energy (p=0.029), carbohydrate (p=0.047), and fructose consumption (p<0.001) were also higher in the SCF group. Multivariable logistic regression analysis demonstrated that a higher level of Hs-CRP, fructose consumption, and smoking were independently associated with SCF. CONCLUSION: The SCF group demonstrated a higher level of fructose consumption. Excessive fructose consumption may play a role in SCF pathophysiology.

Long-Term Follow-Up in Patients With Stable Angina and Unobstructed Coronary Arteries Undergoing Intracoronary Acetylcholine Testing.

OBJECTIVES: The aim of this study was to investigate the prognosis of a large cohort of patients with stable angina and unobstructed coronaries undergoing acetylcholine spasm testing. BACKGROUND: Coronary artery spasm can be found in up to 60% of patients with symptoms of myocardial ischemia despite unobstructed coronary arteries. METHODS: Consecutive symptomatic patients with unobstructed coronary arteries undergoing acetylcholine testing to detect epicardial or microvascular coronary spasm were prospectively enrolled. After a median follow-up period of 7.2 years (6.5 to 7.9 years), data regarding mortality, nonfatal myocardial infarction, stroke, repeat coronary angiography, recurrent symptoms, and quality of life were obtained in 736 patients (57% women, mean age 62 ± 12 years). RESULTS: In total, 55 deaths (7.5%), 8 nonfatal myocardial infarctions (1.4%), and 12 strokes (2.2%) occurred during the follow-up period. Recurrent symptoms were reported by 64% of patients, and repeat coronary angiography was performed in 12% of cases. Multivariate analysis revealed epicardial spasm as a predictor of nonfatal myocardial infarction (hazard ratio: 14.469; 95% confidence interval: 1.735 to 120.646) and repeat angiography (hazard ratio: 1.703; 95% confidence interval: 1.062 to 2.732), whereas patients with microvascular spasm more often had recurrent angina at follow-up (hazard ratio: 1.311; 95% confidence interval: 1.013 to 1.697). CONCLUSIONS: In this long-term follow-up study, the overall prognosis of patients with coronary spasm was favorable. Patients with epicardial spasm were at increased risk for myocardial infarction and repeat angiography, while microvascular spasm was associated with recurrent angina. Acetylcholine testing may help identify patients at increased risk for adverse cardiac events among this overall low-risk population.

Revascularization Deferral of Nonculprit Stenoses on the Basis of Fractional Flow Reserve: 1-Year Outcomes of 8,579 Patients.

BACKGROUND: Intracoronary physiology is increasingly used in nonculprit stenoses of patients with acute coronary syndromes (ACS). However, evidence regarding the safety of fractional flow reserve-based deferral in patients with ACS, compared with patients with stable angina pectoris (SAP), is scarce. OBJECTIVES: The aim of this study was to evaluate the safety of revascularization deferral on the basis of fractional flow reserve interrogation of nonculprit lesions in patients with ACS. METHODS: A pooled analysis was performed of individual patient data included in 5 large international published studies on physiology-guided revascularization. The primary endpoint was major adverse cardiac events (MACE) (a composite of death, nonfatal myocardial infarction, or unplanned revascularization) at 1-year follow-up. Clinical outcomes of patients with ACS and SAP were compared in both the deferred and the revascularized groups. RESULTS: A total of 8,579 patients were included in the analysis, 6,461 with SAP and 2,118 with ACS and nonculprit stenoses. Using fractional flow reserve, revascularization was deferred in 5,129 patients (59.8%) and performed in 3,450 patients (40.2%). In the deferred ACS group, a higher MACE rate was observed compared with the deferred SAP group (4.46% vs. 2.83%; adjusted hazard ratio [HR]: 1.72; 95% confidence interval [CI]: 1.17 to 2.53; p < 0.01). In particular, early unplanned revascularization (3.34% and 2.04% in ACS and SAP; adjusted HR: 1.81; 95% CI: 1.09 to 3.00; p = 0.02) contributed to this excess in MACE but the difference between the ACS and SAP groups did not reach statistical significance. On the contrary, no differences in outcomes linked to clinical presentation were found in treated patients (MACE rate 6.51% vs. 6.20%; adjusted HR: 1.21; 95% CI: 0.88 to 1.26; p = 0.24). CONCLUSIONS: Patients with ACS in whom revascularization of nonculprit lesions was deferred on the basis of fractional flow reserve have more MACE at 1 year compared with patients with SAP with deferred revascularization. Unplanned revascularization mainly contributed to this excess of MACE.

Effect of nicorandil administration on cardiac burden and cardio-ankle vascular index after coronary intervention.

Myocardial injury is a problem associated with percutaneous coronary intervention (PCI). This study aimed to clarify the role of nicorandil administration in preventing myocardial injury. This study included patients with stable angina who underwent PCI from November 2013 to June 2016. Of 58 consecutive patients, the first 20 patients received only saline infusion after PCI (control group); the other 38 patients received a continuous intravenous infusion of nicorandil and saline after PCI (nicorandil group). Troponin I and brain natriuretic peptide (BNP) levels were measured. Vascular parameters, such as blood pressure (BP), cardiac output, cardio-ankle vascular index (CAVI), and estimated systemic vascular resistance (eSVR), were measured. Troponin I of both groups increased 12 h after PCI. Changes in BNP levels between immediately after PCI and 12 h after PCI were significantly higher in the control than in the nicorandil group (10.8 ± 44.2 vs. - 2.6 ± 14.6 pg/ml, p = 0.04). In the nicorandil group, BP, eSVR, and CAVI decreased significantly at 12 h after PCI compared with those immediately after PCI (p < 0.0001), whereas no change was observed in the control group. In a single linear analysis, the change in BP (r = 0.36, p < 0.01) and nicorandil administration (r = - 0.47, p < 0.001) was significantly correlated with the change in CAVI, multiple regression analysis revealed that the changes in CO and eSVR were significant contributing factors for the changes in CAVI. PCI could result in myocardial injury and/or cardiac burden in patients with stable angina. Nicorandil administration after PCI may be effective in relieving the burden by decreasing arterial stiffness (CAVI).

The predictive value of speckle tracking during dobutamine stress echocardiography in patients with chronic stable angina.

OBJECTIVE: Evaluation of the diagnostic value of speckle tracking echocardiography (STE) at rest and during dobutamine stress in predicting the presence and severity of coronary artery disease (CAD) in patients with chronic stable angina. METHODS: A total of 100 patients with chronic stable angina were evaluated using STE at rest and during dobutamine stress to detect the presence, severity, and number of affected coronary arteries. Then, the correlation with the SYNTAX score (SS) was analyzed. RESULTS: STE at stress showed better agreement with coronary angiography (CA) than dobutamine stress echocardiography (DSE) in detecting the presence of coronary artery stenosis (Kappa = 0.819, p < 0.001). STE at stress suggested involvement of the left anterior descending artery (LAD) with excellent agreement with CA (Kappa = 0.816, p < 0.001). For right coronary artery, STE at rest and stress showed good agreement with the CA results (Kappa = 0.775 and 0.858, respectively, p < 0.001), whereas for left circumflex artery, STE at rest and stress showed a fair agreement with the CA results (Kappa = 0.556 and 0.583, respectively, p < 0.001). Resting global longitudinal peak systolic strain (GLPSS) ≥ -15.2% had the best diagnostic accuracy (sensitivity = 61.8%; specificity = 93.5%) in predicting SS > 22. Stress GLPSS ≥ -12.5% had the best diagnostic accuracy (sensitivity = 82.4%; specificity = 78.3%) in predicting SS > 22. CONCLUSION: Speckle tracking during DSE has high sensitivity and specificity for predicting the presence of CAD. It provides quantitative diagnostic information that decreases the false positive and false negative results of DSE.

Systemic Cardiac Troponin T Associated With Incident Atrial Fibrillation Among Patients With Suspected Stable Angina Pectoris.

Higher concentrations of cardiac troponin T are associated with coronary artery disease (CAD) and adverse cardiovascular prognosis. The relation with incident atrial fibrillation (AF) is less explored. We studied this association among 3,568 patients evaluated with coronary angiography for stable angina pectoris without previous history of AF. The prospective association between high-sensitivity cardiac troponin T (hs-cTnT) categories (≤3 ng/L; n = 1,694, 4-9; n = 1,085, 10 to 19; n = 614 and 20 to 30; n = 175) and incident AF and interactions with the extent of CAD were studied by Kaplan-Meier plots and Cox regression. Risk prediction improvements were assessed by receiver operating characteristic area under the curve (ROC-AUC) analyses. During median (25 to 75 percentile) 7.3 (6.3 to 8.6) years of follow-up 412 (11.5%) were diagnosed with AF. In a Cox model adjusted for age, gender, body mass index, hypertension, diabetes mellitus, smoking, estimated glomerular filtration rate, and left ventricular ejection fraction, hazard ratios (HRs) (95% confidence intervals [CIs]) were 1.53 (1.16 to 2.03), 2.03 (1.49 to 2.78), and 2.15 (1.40 to 3.31) when comparing the second, third, and fourth to the first hs-cTnT group, respectively (P for trend <0.000001). The strongest association between hs-cTnT levels and incident AF was found among patients without obstructive CAD (Pint = 0.024) and adding hs-cTnT to established AF risk factors improved risk classification slightly (ΔROC 0.006, p = 0.044). In conclusion, in patients with suspected stable angina higher levels of hs-cTnT predicted increased risk of incident AF. This was most pronounced in patients without obstructive CAD suggesting an association not mediated by coronary disease.

Early diastolic strain rate by two-dimensional speckle tracking echocardiography is a predictor of coronary artery disease and cardiovascular events in stable angina pectoris.

This study aimed to clarify the diagnostic and prognostic potential of strain rate in patients with suspected stable angina pectoris (SAP). Strain rate by 2-dimensional speckle tracking echocardiography (2DSTE) has been suggested to be able to diagnose coronary artery disease (CAD) and predict cardiovascular events in various patient groups. Prospectively enrolled patients (n = 296) with suspected SAP, no previous cardiac disease, and normal left ventricular ejection fraction were examined by 2DSTE, exercise ECG, and coronary angiography. Obstructive CAD was defined as stenosis ≥ 70% in ≥ 1 coronary artery on coronary angiography (n = 107). Major adverse cardiac events (MACE) included myocardial infarction, heart failure, atrial fibrillation, and stroke. In multivariable analysis adjusted for baseline data, conventional echocardiography, and Duke score, early diastolic strain rate (SRe) was independently associated with significant CAD with a 1.35 increased risk of having CAD per 0.1 decrease in SRe (OR = 1.35, 95% CI 1.03-1.76, P = 0.027). Peak velocity of early diastolic filling (E)/SRe was not associated with significant CAD (OR = 1.14, 95% CI 0.81-1.62, P = 0.445). MACE occurred in 34 patients (12%) during follow-up (median 3.5 years) and both SRe (HR 1.26, 95% CI (1.07-1.49), P = 0.006) and E/SRe (HR 1.24, 95% CI (1.04-1.47), P = 0.017) were independent predictors after multivariable adjustment. In patients with suspected SAP, SRe by 2DSTE was independently associated with presence of CAD. In addition, SRe and E/SRe provided independent and incremental prognostic value for predicting future MACE.

Clinical significance of healed plaque detected by optical coherence tomography: a 2-year follow-up study.

Recent studies have shown that healed plaque at the culprit lesion detected by optical coherence tomography (OCT) is a sign of pan-vascular vulnerability and advanced atherosclerosis. However, the clinical significance of healed plaque is unknown. A total of 265 patients who had OCT imaging of a culprit vessel and 2-year clinical follow-up data were included. Patients were stratified based on the presence or absence of a layered plaque phenotype, defined as layers of different optical density by OCT at either culprit or non-culprit lesions. The association between layered plaque and major adverse cardiac events (MACE), defined as cardiac death, acute coronary syndromes (ACS), or revascularization, was studied. Among 265 patients, 96 (36.2%) had the layered plaque phenotype. Layered plaque was more frequently observed in stable angina pectoris patients than in ACS patients (57.8%vs. 25.1%, p < 0.001). The average clinical follow-up period was 672 ± 172 days. Cumulative MACE was significantly higher in patients with layered plaque (p = 0.041), which was primarily driven by the high revascularization rate at 2 years (p = 0.002). Multivariate regression analysis showed that presence of layered plaque and low-density lipoprotein cholesterol levels were independently associated with an increased risk of revascularization (p = 0.026, p = 0.008, respectively). Patients with healed plaque in the culprit vessel had a higher incidence of revascularization, as compared to those without healed plaque, at 2 years.

Predictors for layered coronary plaques: an optical coherence tomography study.

Healed coronary plaques, morphologically characterized by a layered pattern, are signatures of previous plaque disruption and healing. Recent optical coherence tomography (OCT) studies showed that layered plaque is associated with vascular vulnerability. However, factors associated with layered plaques have not been studied. The aim of this study was to investigate predictors for layered plaque at the culprit plaques and at non-culprit plaques. Patients with coronary artery disease who underwent pre-intervention OCT imaging of the culprit lesion were included. Layered plaques were defined as plaques with one or more layers of different optical density and a clear demarcation from underlying components. Among 313 patients, layered plaque at the culprit lesion was observed in 18.8% of ST-segment elevation myocardial infarction patients, 36.3% of non-ST-segment elevation acute coronary syndrome patients, and 53.4% of stable angina pectoris (SAP) patients (p < 0.001). In the multivariable model, SAP, multivessel disease, type B2/C lesion, and diameter stenosis > 70% were independent predictors for layered plaque at the culprit lesion. In addition, 394 non-culprit plaques in 190 patients were assessed to explore predictors for layered plaques at non-culprit lesions. SAP, and thin-cap fibroatheroma and layered plaque at the culprit lesion were independent predictors for layered plaques at non-culprit lesions. In conclusion, clinical presentation of SAP was a strong predictor for layered plaque at both culprit plaques and non-culprit plaques. Development and biologic significance of layered plaques may be related to a balance between pan-vascular vulnerability and endogenous anti-thrombotic protective mechanism.