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Editorials, ischemia, mortality, myocardial ischemia, coronary angiography Keywords: Editorials; coronary angiography; ischemia; mortality; myocardial ischemia EN Editorials coronary angiography ischemia mortality myocardial ischemia 20 22 3 12/29/22 20230103 NES 230103 B Article, see p 8 b According to the ancient Greeks, the lives of the gods and mortals were immutably determined by 3 Fates: sisters Clotho, who spins the thread of life; Lachesis, who assigns each their destiny; and Atropos, whose scissors snip the thread of life at its end. Analyses from ISCHEMIA,[10] and COURAGE before it,[11] have demonstrated a time-dependent effect of an invasive strategy on patient-reported health status, most notably symptom burden among patients with more severe anginal symptoms at baseline. [Extracted from the article]

Background: Representation by age ensures appropriate translation of clinical trial results to practice, but, historically, older patients have been underrepresented in clinical trial populations. As the general population has aged, it is unknown whether clinical trial enrollment has changed in parallel. Methods and Results: We studied time trends in enrollment, clinical characteristics, treatment, and outcomes by age among 76 141 patients with non-ST-segment-elevation acute coronary syndrome enrolled in 11 phase III clinical trials over 17 years (1994-2010). Overall, 19.7% of patients were ≥75 years; this proportion increased from 16% during 1994 to 1997 to 21% during 1998 to 2001 and 23.2% during 2002 to 2005, but declined to 20.2% in 2006 to 2010. The number of comorbidities increased with successive time periods irrespective of age. There were substantial increases in the use of evidence-based medication in-hospital and at discharge regardless of age. Although predicted 6-month mortality increased slightly over time, observed 6-month mortality declined significantly in all age strata (1994-1997 versus 2006-2010: <65 years: 3.0% versus 1.9%; 65-74 years: 7.5% versus 3.4%; 75-79 years: 13.0% versus 6.5%; 80-84 years: 17.6% versus 8.2%; and ≥85 years: 24.8% versus 12.6%). Conclusions: The distribution of enrollment by age in phase III non-ST-segment-elevation acute coronary syndrome trials was unchanged over time. Irrespective of age, post-myocardial infarction mortality decreased significantly over time, concurrent with increased evidence-based care and despite increasing comorbidities. Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00089895. [ABSTRACT FROM AUTHOR]

Background: Few studies have used individual person data to study whether contemporary trends in the incidence of coronary heart disease are associated with changes in modifiable coronary risk factors.Methods and Results: We identified 29 582 healthy men and women ≥25 years of age who participated in 3 population surveys conducted between 1994 and 2008 in Tromsø, Norway. Age- and sex-adjusted incidence rates were calculated for coronary heart disease overall, out-of-hospital sudden death, and hospitalized ST-segment-elevation and non-ST-segment-elevation myocardial infarction. We measured coronary risk factors at each survey and estimated the relationship between changes in risk factors and changes in incidence trends. A total of 1845 participants had an incident acute coronary heart disease event during 375 064 person-years of follow-up from 1994 to 2010. The age- and sex-adjusted incidence of total coronary heart disease decreased by 3% (95% confidence interval, 2.0-4.0; P<0.001) each year. This decline was driven by decreases in out-of-hospital sudden death and hospitalized ST-segment-elevation myocardial infarction. Changes in coronary risk factors accounted for 66% (95% confidence interval, 48-97; P<0.001) of the decline in total coronary heart disease. Favorable changes in cholesterol contributed 32% to the decline, whereas blood pressure, smoking, and physical activity each contributed 14%, 13%, and 9%, respectively.Conclusions: We observed a substantial decline in the incidence of coronary heart disease that was driven by reductions in out-of-hospital sudden death and hospitalized ST-segment-elevation myocardial infarction. Changes in modifiable coronary risk factors accounted for 66% of the decline in coronary heart disease events. [ABSTRACT FROM AUTHOR]

Background-Emergency coronary artery bypass grafting for unsuccessful percutaneous coronary intervention (PCI) is now rare. We aimed to evaluate the current safety and outcomes of primary PCI and nonprimary PCI at centers with and without on-site surgical backup. Methods and Results-We performed an updated systematic review and meta-analysis by using mixed-effects models. We included 23 high-quality studies that compared clinical outcomes and complication rates of 1 101 123 patients after PCI at centers with or without on-site surgery. For primary PCI for ST-segment-elevation myocardial infarction (133 574 patients), all-cause mortality (without on-site surgery versus with on-site surgery: observed rates, 4.8% versus 7.2%; pooled odds ratio [OR], 0.99; 95% confidence interval, 0.91-1.07; P=0.729; I2=3.4%) or emergency coronary artery bypass grafting rates (observed rates, 1.5% versus 2.4%; pooled OR, 0.76; 95% confidence interval, 0.56-1.01; P=0.062; I2=42.5%) did not differ by presence of on-site surgery. For nonprimary PCI (967 549 patients), all-cause mortality (observed rates, 1.6% versus 2.1%; pooled OR, 1.15; 95% confidence interval, 0.94-1.41; P=0.172; I2=67.5%) and emergency coronary artery bypass grafting rates (observed rates, 0.5% versus 0.8%; pooled OR, 1.14; 95% confidence interval, 0.62-2.13; P=0.669; I2=81.7%) were not significantly different. PCI complication rates (cardiogenic shock, stroke, aortic dissection, tamponade, recurrent infarction) also did not differ by on-site surgical capability. Cumulative meta-analysis of nonprimary PCI showed a temporal decrease of the effect size (OR) for all-cause mortality after 2007. Conclusions-Clinical outcomes and complication rates of PCI at centers without on-site surgery did not differ from those with on-site surgery, for both primary and nonprimary PCI. Temporal trends indicated improving clinical outcomes in nonprimary PCI at centers without on-site surgery. [ABSTRACT FROM AUTHOR]

Background—Myocardial infarction with nonobstructive coronary arteries (MINOCA) is a puzzling clinical entity with no previous evaluation of the literature. This systematic review aims to (1) quantify the prevalence, risk factors, and 12-month prognosis in patients with MINOCA, and (2) evaluate potential pathophysiological mechanisms underlying this disorder. Methods and Results—Quantitative assessment of 28 publications using a meta-analytic approach evaluated the prevalence, clinical features, and prognosis of MINOCA. The prevalence of MINOCA was 6% [95% confidence interval, 5%-7%] with a median patient age of 55 years (95% confidence interval, 51-59 years) and 40% women. However, in comparison with those with myocardial infarction associated with obstructive coronary artery disease, the patients with MINOCA were more likely to be younger and female but less likely to have hyperlipidemia, although other cardiovascular risk factors were similar. All-cause mortality at 12 months was lower in MINOCA (4.7%; 95% confidence interval, 2.6%-6.9%) compared with myocardial infarction associated with obstructive coronary artery disease (6.7%, 95% confidence interval, 4.3%-9.0%). Qualitative assessment of 46 publications evaluating the underlying pathophysiology responsible for MINOCA revealed the presence of a typical myocardial infarct on cardiac magnetic resonance imaging in only 24% of patients, with myocarditis occurring in 33% and no significant abnormality in 26%. Coronary artery spasm was inducible in 27% of MINOCA patients, and thrombophilia disorders were detected in 14%. Conclusions—MINOCA should be considered as a working diagnosis with multiple potential causes that require evaluation so that directed therapies may improve its guarded prognosis. [ABSTRACT FROM AUTHOR]

The article discusses the sedentary behavior of chronic subclinical myocardial injury. Topics mention including the effects of a higher level of physical activity on troponin levels, association of increase sedentary time with increase cause of mortality and connection of chronic myocardial injury with increase sedentary time.

Introduction: There is a lack of data on outcomes in low-flow, low-gradient aortic stenosis (LFLG-AS) patients undergoing TAVR. We aim to compare baseline characteristic and procedural outcomes between LFLG-AS and high-gradient aortic stenosis (HG-AS) patients undergoing TAVR. Hypothesis: TAVR is feasible in LFLG-AS and the outcomes are similar to HG-AS. Methods: Multicentric Latin-American registry of severe aortic stenosis patients undergoing TAVR between 2009 and 2018. Patients were considered HG-AS if mean transaortic gradient (MG) ≥ 40 mmHg and LFLG-AS if MG < 40 mmHg. The outcomes were evaluated at 30-days and were classified according to definitions of the Valve Academic Research Consortium-2. Results: 714 patients were included, 199 (27%) classified as LFLG-AS and 515 (70%) as HG-AS. LFLG-AS patients were more symptomatic (NYHA class III/IV: 75 vs 64%; p=0.006), with higher prevalence of coronary artery disease (59 vs 48%; p=0.012) and previous pacemaker (19 vs 6%; p<0.001) than HG-AS patients. LFLG-AS patients had also lower left ventricular ejection fraction (49±15 vs 56±11%; p<0.001), lower aortic valve area (0.73±0.26 vs 0.66±0.16 cm2; p<0.001), with a MG of 30±7 vs 53±13 mmHg, respectively, with p<0.001, vs. HG-AS. After TAVR, LFLG-AS patients had higher need for vasoactive drugs (17 vs 10%; p=0.010), yet in-hospital mortality (7 vs 5%; p=0.393) and device success rates (71 vs 66%; p=0.158) were similar between both groups. By multivariate analysis, major vascular complication (OR 8.30, 95% CI 1.82-37.75, p=0.006), post-procedure myocardial infarction (OR 21.09, 95% CI 1.18-376.09, p=0.038) and STS score (OR 1.06, 95% CI 1.00-1.13, p=0.030) were associated with 30-day mortality in LFLG-AS. Furthermore, percutaneous access (OR 11.75, 95% CI 7.33-18.84, p<0.001) and procedure contrast amount (OR 1.00, 95% CI 1.00-1.01, p<0.001) were the only predictors of device success in LFLG-AS patients in the multivariate analysis. Conclusion: Apart from baseline differences, TAVR in LFLG-AS was feasible and with similar outcomes when compared to HG-AS. Short-term mortality was associated with procedure complications and STS score, while device success was associated with percutaneous access and contrast amount. [ABSTRACT FROM AUTHOR]

Introduction: Patients with heart failure (HF) are classified as ischemic or non-ischemic according to the underlying etiology. This binary classification combines individuals with non-obstructive coronary artery disease (CAD) with those with apparent normal coronaries under the non-ischemic label. Our objective was to examine the prognostic significance of non-obstructive CAD in patients with HF, treating non-obstructive disease as a distinct category apart from those with normal coronaries. Methods: We conducted a retrospective cohort study using the CorHealth Cardiac Registry, which collects clinical and coronary anatomical data for individuals undergoing invasive cardiac catheterization in Ontario, Canada. We included individuals with reduced left ventricular ejection fraction (<35%), no previous revascularization, and no recent acute myocardial infarction (AMI) between 2010 and 2015. We divided patients in three groups according to the severity of CAD: normal coronaries (0% stenosis); non-obstructive disease (1-69%); and significant disease (≥70%). The cohort was linked to administrative databases for outcomes evaluation. Results: We examined 13,575 individuals of whom 2837 (20.9%) had normal coronary anatomy, 2422 (17.8%) had non-obstructive disease, and 8316 (61.3%) had significant disease. The rate of death due to any cause was increased in the non-obstructive group (adjusted hazard ratio {HR} 1.14, 95% confidence interval {CI} 1.04-1.24, P=0.006) relative to those with normal coronaries (Figure). Non-obstructive CAD was also associated with an increased hazard of death or AMI (HR 1.23, 95% CI; 1.10-1.38, P<0.001), death or HF hospitalization (HR 1.10; 95% CI 1.01-1.19; P =0.03), and death or hospitalization for AMI, HF, or stroke (HR 1.15; 95% CI 1.04-1.26; P =0.005). Conclusions: Non-obstructive CAD was independently associated with an increased hazard of experiencing death or cardiovascular events among individuals with reduced left ventricular ejection fraction. [ABSTRACT FROM AUTHOR]

Background: Recent basic studies suggests the importance of lymphatic vasculature as a therapeutic target in cardiovascular diseases. Treatment with vascular endothelial growth factor-C (VEGF-C), a central player in lymphangiogenesis, after myocardial infarction induces lymphangiogenesis, reduces fluid retention, facilitates inflammatory cell clearance in the cardiac tissue, and improves cardiac function. However, the relationship between VEGF-C and mortality in patients with stable coronary artery disease (CAD) and a history of heart failure is unknown. Methods: Serum VEGF-C levels were measured in 152 patients with stable CAD and a history of heart failure, enrolled in the development of novel biomarkers related to angiogenesis or oxidative stress to predict cardiovascular events (ANOX) study, and followed up for 3 years. The outcomes were all-cause and cardiovascular deaths. Results: During the follow-up, 45 patients (30%) died from any cause, and 20 (13%) died from cardiovascular disease. After adjustment for established risk factors, the lowest quartile of VEGF-C was significantly associated with all-cause death (hazard ratio [HR] for for values below the 25th percentile, 2.7; 95% confidence interval [CI], 1.4-5.4) and cardiovascular death (HR for values below the 25th percentile, 5.8; 95% CI, 2.2-17). Even after additional adjustment of N-terminal pro-brain natriuretic peptide, contemporary sensitive cardiac troponin-I, and high-sensitivity C-reactive protein, lowest quartile of VEGF-C was significantly associated with all-cause death (HR, 2,2; 95% CI, 1.1-4.4) and cardiovascular death (HR, 3.7; 95% CI, 1.3-11). Conclusions: In patients with stable CHD and a history of heart failure, a low VEGF-C value may predict all-cause and cardiovascular mortality independent of established risk factors and standard cardiovascular biomarkers. [ABSTRACT FROM AUTHOR]

Background: Growth differentiation factor-15 (GDF-15) is a stress-responsive cytokine, which plays an important role in the regulation of the inflammatory response, growth and cell differentiation. Elevated GDF-15 was found in various diseases including chronic kidney disease (CKD) and stable coronary heart disease (CHD), and was reported to predict mortality and cardiovascular events in general or established CHD population. However, the predictive value of GDF-15 in patients with CKD and stable CHD remains to be determined. Methods: Serum GDF-15 levels were measured in 664 patients with CKD and stable CHD, enrolled in the development of novel biomarkers related to angiogenesis or oxidative stress to predict cardiovascular events (ANOX) study, and followed up for 3 years. The primary outcome was all-cause death. The secondary outcomes were cardiovascular death, and a major adverse cardiovascular event (MACE) defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke. Results: During the follow-up, 119 patients died from any cause, 47 died from cardiovascular disease, and 75 developed MACE. After adjustment for established risk factors, GDF-15 levels were significantly associated with all-cause death (hazard ratio [HR] for 1-SD increase, 1.76; 95% confidence interval [CI], 1.52-2.03), cardiovascular death (HR, 1.78; 95% CI, 1.43-2.19), and MACE (HR, 1.51; 95% CI, 1.25-1.81). Even after incorporation of N-terminal pro-brain natriuretic peptide, contemporary sensitive cardiac troponin-I, and high-sensitivity C-reactive protein into a model with established risk factors, the addition of GDF-15 levels further improved the prediction of all-cause death (continuous net reclassification improvement, 0.32; 95% CI, 0.13-0.52; P =0.001; integrated discrimination improvement, 0.03; 95% CI, 0.01-0.04; P =0.01), but not that of cardiovascular death or MACE. Conclusions: In patients with CKD and stable CHD, elevated GDF-15 levels predicted all-cause mortality, but not cardiovascular mortality or MACE, independent of established risk factors and standard cardiovascular biomarkers. [ABSTRACT FROM AUTHOR]

Background: Growth differentiation factor-15 (GDF-15) is a stress-responsive cytokine, which plays an important role in the regulation of the inflammatory response, growth and cell differentiation. Elevated GDF-15 was found in various diseases including diabetes and stable coronary heart disease (CHD), and was reported to predict mortality and cardiovascular events in general or established CHD population. However, the predictive value of GDF-15 in patients with diabetes and stable CHD is yet to be determined. Methods: Serum GDF-15 levels were measured in 797 patients with diabetes and stable CHD, enrolled in the development of novel biomarkers related to angiogenesis or oxidative stress to predict cardiovascular events (ANOX) study, and followed up for 3 years. The primary outcome was all-cause death. The secondary outcomes were cardiovascular death, and a major adverse cardiovascular event (MACE) defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke. Results: During the follow-up, 121 patients died from any cause, 42 died from cardiovascular disease, and 85 developed MACE. After adjustment for established risk factors, GDF-15 levels were significantly associated with all-cause death (hazard ratio [HR] for 1-SD increase, 1.74; 95% confidence interval [CI], 1.52-1.98), cardiovascular death (HR, 1.59; 95% CI, 1.26-1.96), and MACE (HR, 1.39; 95% CI, 1.16-1.64). Even after incorporation of N-terminal pro-brain natriuretic peptide, contemporary sensitive cardiac troponin-I, and high-sensitivity C-reactive protein into a model with established risk factors, the addition of GDF-15 levels further improved the prediction of all-cause death (continuous net reclassification improvement [NRI], 0.44; 95% CI, 0.24-0.63; P <0.001; integrated discrimination improvement [IDI], 0.05; 95% CI, 0.03-0.08; P <0.001), cardiovascular death (NRI, 0.23; 95% CI, 0.02-0.44; P =0.03; IDI, 0.03; 95% CI, 0.01-0.05; P =0.001), and MACE (NRI, 0.18; 95% CI, 0.02-0.34; P =0.03; IDI, 0.01; 95% CI, 0.001-0.02; P =0.03). Conclusions: In patients with diabetes and stable CHD, elevated GDF-15 levels predicted all-cause and cardiovascular mortality, and MACE, independent of established risk factors and standard cardiovascular biomarkers. [ABSTRACT FROM AUTHOR]

Introduction: Use of high-sensitivity troponin (hsTn) in stable patients (pts) with established ischemic heart disease (SIHD) is an emerging application to identify heightened risk of major cardiovascular (CV) events. However, appropriate decision-limits are not yet defined. Methods: We measured serum hsTnI (Abbott ARCHITECT, limit-of-detection 2 ng/L, MI cut-point 26 ng/L) in a prospective nested cohort of 8,635 pts enrolled in the PEGASUS-TIMI 54 trial. All patients had SIHD with a myocardial infarction (MI) 1-3 years prior to enrollment. Previous studies have proposed 6 ng/L as a decision-limit for risk stratification. Pts were categorized based on baseline hsTnI: undetectable (<2), low (2-6), and high (>6 ng/L). The primary endpoint (PEP) was a composite of CV death, MI, or stroke. Pts were followed for a median of 33 months. Results: The median value of hsTnI was 4.2 ng/L (25th, 75th: 2.7, 7.2 ng/L) and 89.3% of pts had detectable hsTnI (≥2 ng/L) with 31.1% >6 ng/L. The 3y PEP rates for the undetectable, low, and high hsTnI groups were 2.8, 6.0, and 13.5%, respectively (Fig). Adjusting for age, diabetes, smoking, hypertension, stroke, CABG, peripheral artery disease, history of heart failure and chronic kidney disease, there remained a 2 and 4-fold higher risk for the PEP in the low and high hsTnI groups(Fig). Rates of MI in the undetectable, low, and high groups were 2.5, 4.3, and 8.7%, respectively, with adjusted HRs of 1.9 (95% CI 1.2-3.2, p=0.009) in the low and 3.6 (95% CI 2.2-6.0, p<0.0001) in the high group. No CV deaths occurred in pts with undetectable troponin. There was no significant interaction with efficacy of ticagrelor. Conclusion: hsTn demonstrates a strong independent graded association with recurrent major cardiovascular events in pts with SIHD. The increased risk is present in the low detectable range and progresses with higher levels. A single hsTnI >6 ng/L was present in nearly 1/3 of patients, identifying a 4-fold higher risk of recurrent cardiac event. [ABSTRACT FROM AUTHOR]

Introduction: There remains debate in terms of appropriate target of blood glucose levels particularly in type 2 diabetic patients with long history of diabetes and co-morbidities. We explored the association of hemoglobin A1c levels with cardiovascular outcome and mortality. Hypothesis: Achieved hemoglobin A1c levels are associated with death, myocardial infarction and stroke in Japanese patients with type 2 diabetes and coronary artery disease. Methods: We consecutively registered 7785 type 2 diabetes patients with established coronary artery disease from records of coronary angiography at each hospital since 2006 and followed up through 2017. The primary composite outcome was all-cause death, non-fatal myocardial infarction and non-fatal stroke. Association of hemoglobin A1c during the follow up period with the primary composite outcome and each end point was evaluated by deriving hazard ratios of patients whose averaged hemoglobin A1c were below 6%, 7% to 8%, above 8% to those who with 6% to 7% using Cox proportional hazard model. Results: A total of 28531 patients-years of follow-up provided 1414 primary outcomes. In terms of the primary composite end point, risks in patients with either above 8% of hemoglobin A1c (hazard ratio 1.36, 95%confidence interval 1.16 to 1.60, p=0.0002) or below 6% (hazard ratio 1.23, 95%confidence interval 1.02 to 1.48, p=0.0273) were significantly higher than in those with 6-7%. Risks for total mortality was similarly and significantly higher in either below 6% and above 8%. On the other hand, risks for fatal and non-fatal myocardial infarction were significantly higher in 7-8% (hazard ratio 1.44, 95%confidence interval 1.03 to 2.00, p=0.0315) and above 8% (hazard ratio 1.58, 95%confidence interval 1.08 to 2.33, 0.0197) than in 6-7%. Conclusions: Results from our retrospective cohort study in type 2 diabetic patients with coronary heart disease suggest that the relationship between mortality and achieved glycemic controls shows U shaped curve while risk for myocardial infarction appears to show positive correlation. Hemoglobin A1c being 6 to 7% seems to be justified as appropriate target glycemic control but cause of excess mortality in patients with below 6% should be investigated. [ABSTRACT FROM AUTHOR]