Myocardial Infarction incidence during national lockdown in two French provinces unevenly affected by COVID-19 outbreak: An observational study.

BACKGROUND: A reduction of admission for MI has been reported in most countries affected by COVID-19. No clear explanation has been provided. METHODS: To report the incidence of myocardial infarction (MI) admission during COVID-19 pandemic and in particular during national lockdown in two unequally affected French provinces (10-million inhabitants) with a different media strategy, and to describe the magnitude of MI incidence changes relative to the incidence of COVID-19-related deaths. A longitudinal study to collect all MIs from January 1 until May 17, 2020 (study period) and from the identical time period in 2019 (control period) was conducted in all centers with PCI-facilities in northern "Hauts-de-France" province and western "Pays-de-la-Loire" Province. The incidence of COVID-19 fatalities was also collected. FINDINGS: In "Hauts-de-France", during lockdown (March 18-May 10), 1500 COVID-19-related deaths were observed. A 23% decrease in MI-IR (IRR=0.77;95%CI:0.71-0.84, p<0.001) was observed for a loss of 272 MIs (95%CI:-363,-181), representing 18% of COVID-19-related deaths. In "Pays-de-la-Loire", 382 COVID-19-related deaths were observed. A 19% decrease in MI-IR (IRR=0.81; 95%CI=0.73-0.90, p<0.001) was observed for a loss of 138 MIs (95%CI:-210,-66), representing 36% of COVID-19-related deaths. While in "Hauts-de-France" the MI decline started before lockdown and recovered 3 weeks before its end, in "Pays-de-la-Loire", it started after lockdown and recovered only by its end. In-hospital mortality of MI patients was increased during lockdown in both provinces (5.0% vs 3.4%, p=0.02). INTERPRETATION: It highlights one of the potential collateral damages of COVID-19 outbreak on cardiovascular health with a dramatic reduction of MI incidence. It advocates for a careful and weighted communication strategy in pandemic crises. FUNDING: The study was conducted without external funding.

Radial versus femoral access for coronary angiography and intervention is associated with lower patient radiation exposure in high-radial-volume centres: Insights from the RAY'ACT-1 study.

BACKGROUND: Literature suggests that radial access is associated with higher radiation doses than femoral access. AIMS: To compare patient radiation exposure during coronary angiography (CA) and percutaneous coronary intervention (PCI) with radial versus femoral access. METHODS: RAY'ACT is a nationwide, multicentre, French survey evaluating patient radiation in interventional cardiology. Variables of patient exposure from 21,675 CAs and 17,109 PCIs performed at 44 centres during 2010 were analysed retrospectively. RESULTS: Radial access was used in 71% of CAs and 69% of PCIs. Although median fluoroscopy times were longer for radial versus femoral access (CA, 3.8 vs 3.5minutes [P<0.001]; PCI, 10.4 vs 10.1minutes [P=0.001]), the Kerma-area product (KAP) was lower with radial access (CA, 26.8 vs 28.1Gy·cm2; PCI, 55.6 vs 59.4Gy·cm2; both P=0.001). Differences in KAP remained significant in the multivariable analysis (P<0.01), and in a propensity score-matched analysis (P=0.01). A significant interaction was found between KAP and the percentage of procedures with radial access by centre (P<0.001). KAP was higher by radial versus femoral access in low-radial-volume centres, and lower in high-radial-volume centres. Radiation protection techniques, such as the use of low frame rates (7.5 frame/s), were used more frequently in high-radial-volume radial centres. CONCLUSIONS: In this multicentre study, radial access was associated with lower radiation doses to patient than femoral access in high-radial-volume centres. Provided that radioprotection methods are implemented, radial access could be associated with lower patient radiation exposure.

Dual antiplatelet therapy in patients with stable coronary artery disease in modern practice: prevalence, correlates, and impact on prognosis (from the Suivi d'une cohorte de patients COROnariens stables en region NORd-Pas-de-Calais study).

BACKGROUND: The prevalence and correlates of dual-antiplatelet therapy (DAPT) use in stable coronary artery disease (CAD) are unknown. In addition, whether prolonged DAPT may impact prognosis in stable CAD has not been studied in real-life conditions. METHODS: We studied 3,691 patients included in a prospective registry on stable CAD. The patients were divided in 2 groups according to their antiplatelet therapy regimen at inclusion: patients treated with DAPT were compared with those treated with single-antiplatelet therapy (SAPT). The primary outcome was a composite of cardiovascular death, myocardial infarction, or stroke. RESULTS: Altogether, 868 (24%) patients received DAPT. Factors positively associated with DAPT use were persistent angina at inclusion, body mass index, myocardial infarction since 1 to 3 years, myocardial revascularization since 1 to 3 years, multivessel CAD, prior drug-eluting stent implantation, and prior aortic or peripheral intervention. Factors negatively associated with DAPT use were age, prior coronary bypass, and left ventricular ejection fraction. The rate of the primary outcome at 2 years was similar whether patients were treated with SAPT (4.6%) or DAPT (5.5%) (P = .301). Similar rates were also observed after propensity score matching: 5.7% when treated with SAPT versus 5.5% when treated with DAPT (P = .886). The rate of bleeding was similar between groups. CONCLUSIONS: Our study shows that a significant proportion of stable CAD patients are treated with DAPT in modern practice. Several correlates of DAPT were identified. Although no increase in bleeding was observed, our results do not support the prescription of prolonged DAPT.

Usefulness of serial assessment of B-type natriuretic peptide, troponin I, and C-reactive protein to predict left ventricular remodeling after acute myocardial infarction (from the REVE-2 study).

Left ventricular (LV) remodeling after myocardial infarction (MI) indicates a high risk of heart failure and death. However, LV remodeling is difficult to predict, and limited information is available on the association of cardiac biomarkers with LV remodeling. Our aim was to study the association of B-type natriuretic peptide (BNP), cardiac troponin I (cTnI), and C-reactive protein with LV remodeling after MI. We designed a prospective multicenter study including 246 patients with a first anterior Q-wave MI. Serial echocardiographic studies were performed at hospital discharge and 3 months and 1 year after MI; quantitative analysis was performed at a core echocardiographic laboratory. Blood samples for determination of BNP, cTnI, and C-reactive protein levels were obtained at hospital discharge and the 1-month, 3-month, and 1-year follow up visits. One-year echocardiographic follow-up was obtained in 226 patients. End-diastolic volume increased from 52.3 ± 13.8 ml/m(2) at baseline to 62.3 ± 18.4 ml/m(2) at 1 year (p <0.0001); LV remodeling (>20% increase in end-diastolic volume) was observed in 87 patients (38%). At baseline, we found significant univariate relations between LV remodeling and the 3 biomarkers. During follow-up, high BNP levels and persistently detectable levels of cTnI were associated with LV remodeling. In multivariate analysis, none of the 3 biomarkers at baseline was independently predictive of LV remodeling. In contrast, during follow-up, high BNP and positive cTnI were independently associated with LV remodeling. In conclusion, circulating cardiac biomarkers may reflect pathophysiologic processes implicated in LV remodeling after MI. Determination of BNP and cTnI during follow-up can help refine risk stratification.

The effect of ageing on cardiac remodelling and hospitalization for heart failure after an inaugural anterior myocardial infarction.

AIMS: Following myocardial infarction (MI), both age and left ventricular (LV) remodelling are associated with an increased risk of adverse events. We tested the hypothesis that the increased incidence of heart failure following MI in elderly patients is associated with a greater propensity for LV remodelling. METHODS AND RESULTS: We monitored 266 patients with anterior MI. Echocardiographic studies were performed at hospital discharge, at 3 months, and at 1 year following hospitalization for MI. A clinical follow-up examination was performed after 3 years. Left ventricular remodelling was documented by an increase in LV end-diastolic volume after 1 year. Left ventricular end-diastolic and end-systolic volumes did not differ with age for all time points studied. Left ventricular remodelling was observed in 31, 26, 34, and 34% of patients <48, 48-57, 58-71, and >71 years of age, respectively. The 3 year heart-failure hospitalization rates were 1.9, 1.5, 11.0, and 20.3% for patients <48, 48-57, 58-71, and >71 years of age, respectively. Hospitalization for heart failure was more frequent in older patients. CONCLUSION: We found that age was a major determinant of subsequent re-hospitalization for heart failure. However, we found no significant association between age and the LV remodelling process.

A prospective evaluation of left ventricular remodeling after inaugural anterior myocardial infarction as a function of gene polymorphisms in the renin-angiotensin-aldosterone, adrenergic, and metalloproteinase systems.

BACKGROUND: Left ventricular remodeling (LVR) is a strong predictor of cardiovascular events after myocardial infarction (MI). Although several factors have been shown to influence LVR, interindividual variability exists. Some studies have suggested that gene polymorphisms may be associated with LVR, but these studies were limited by either a retrospective design or the inclusion of limited patient numbers. The present study was designed to prospectively assess the impact of gene polymorphisms on LVR. METHODS: We included 266 patients with inaugural anterior MI. Systematic echocardiographic follow-ups were performed at 3 months and at 1 year after MI. The polymorphisms were selected using a candidate gene approach based on LVR pathophysiology. We analyzed 14 polymorphisms in 3 different systems: the renin-angiotensin-aldosterone system (ACE I/D, RAT1 1166A/C, angiotensinogen M235T, CYP11B2 -344C/T), the adrenergic system (beta1AR Ser49Gly, beta1AR Gly389Arg, beta2AR Gly16Arg, beta2AR Gln27Glu, beta2AR Thr164Ile, alpha2cAR Del322-325), and the metalloproteinase (MMP) system (-1607 1G/2G MMP-1, -1306 C/T MMP-2, -1171 5A/6A MMP-3, -1562 C/T MMP-9). RESULTS: Left ventricular remodeling was documented by a progressive increase in end-diastolic volume from 56.5 +/- 14.9 mL/m2 at baseline to 62.8 +/- 18.8 mL/m2 at 1 year (P < .0001). End-diastolic volume at baseline, 3 months, or 1 year did not differ significantly among genotypes for any polymorphism. The change in end-diastolic volume from baseline to 1 year was also similar among genotypes for all polymorphisms. CONCLUSIONS: Left ventricular remodeling after MI is not associated with common polymorphisms in the renin-angiotensin-aldosterone, adrenergic, or MMP systems.

Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] study group).

Left ventricular (LV) remodeling after acute myocardial infarction (AMI) has been well described in previous studies. However, there is a paucity of data on the incidence of and risk factors for LV remodeling in modern clinical practice that incorporates widespread use of acute reperfusion strategies and almost systematic use of "antiremodeling" medications, such as angiotensin-converting enzyme inhibitors and beta blockers. We enrolled 266 patients with anterior wall Q-wave AMI who had >or=3 segments of the infarct zone that were akinetic on echocardiography before discharge. Echocardiographic follow-up was performed 3 months and 1 year after AMI. LV volumes, ejection fraction, wall motion score index, and mitral flow velocities were determined in a blinded analysis at a core echocardiographic laboratory. Acute reperfusion was attempted in 220 patients (83%; primary angioplasty in 29% and thrombolysis in 54%). During hospitalization, 99% of patients underwent coronary angiography and 87% underwent coronary stenting of the infarct-related lesion. At 1 year, 95% of patients received an antiplatelet agent, 89% a beta blocker, 93% an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker, and 93% a statin. Echocardiographic follow-up was obtained in 215 patients. There was recovery in LV systolic function as shown by a decrease in wall motion score index and an increase in ejection fraction. There was a significant increase in end-diastolic volume (EDV; 56.4 +/- 14.7 ml/m2 at baseline, 59.3 +/- 15.7 ml/m2 at 3 months, 62.8 +/- 18.7 ml/m2 at 1 year, p <0.0001). LV remodeling (>20% increase in EDV) was observed in 67 patients (31%). Peak creatine kinase level, systolic blood pressure, and wall motion score index were independently associated with changes in EDV. In conclusion, recent improvements in AMI management do not abolish LV remodeling, which remains a relatively frequent event after an initial anterior wall AMI.