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Proper prescription and high adherence to intensive lipid lowering drugs (LLD) in patients with coronary heart disease (CHD) are crucial and strongly recommended. The aim of this study is to investigate long-term treatment patterns and adherence to LLD following hospitalization for a CHD event. Patients admitted to two Norwegian hospitals with a CHD event from 2011 to 2014 (N = 1094) attended clinical examination and completed a questionnaire, median 16 months later. Clinical data were linked to pharmacy dispensing data from 2010 to 2020. The proportions using high-intensity statin therapy (atorvastatin 40/80 mg or rosuvastatin 20/40 mg) and non-statin LLD after the CHD event were assessed. Adherence was evaluated by proportion of days covered (PDC) and gaps in treatment. Median age at hospitalization was 63 (IQR 12) years, 21 % were female. Altogether, 1054 patients (96 %) were discharged with a statin prescription, while treatment was dispensed in 85 % within the following 90 days. During median 8 (SD 2.5) years follow-up, the proportion using high-intensity statin therapy ranged 62–68 %, whereas the use of ezetimibe increased from 4 to 26 %. PDC <0.8 was found in 22 % of statin users and 26 % of ezetimibe users. The proportions with a treatment gap exceeding 180 days were 22 % for statins and 28 % for ezetimibe. Smoking at hospitalization and negative affectivity were significantly associated with reduced statin adherence, regardless of adherence measure. In this long-term follow-up of patients with CHD, less than 70 % used high-intensity statin therapy with only small changes over time, and only 25 % used additional treatment with ezetimibe. We identified factors associated with reduced statin adherence that may be target for interventions. [Display omitted] • Less than 70 % of patients with coronary heart disease used high-intensity statin therapy with only small changes over time. • Only one in four patients used additional treatment with ezetimibe. • More than one in five had poor long-term adherence to lipid lowering drugs. • There is a major potential for improving long-term lipid management in secondary prevention. [ABSTRACT FROM AUTHOR]

Background: Lipoprotein(a) concentration is associated with cardiovascular events. Alirocumab, a proprotein convertase subtilisin/kexin type 9 inhibitor, lowers lipoprotein(a) and low-density lipoprotein cholesterol (LDL-C).Objectives: A pre-specified analysis of the placebo-controlled ODYSSEY Outcomes trial in patients with recent acute coronary syndrome (ACS) determined whether alirocumab-induced changes in lipoprotein(a) and LDL-C independently predicted major adverse cardiovascular events (MACE).Methods: One to 12 months after ACS, 18,924 patients on high-intensity statin therapy were randomized to alirocumab or placebo and followed for 2.8 years (median). Lipoprotein(a) was measured at randomization and 4 and 12 months thereafter. The primary MACE outcome was coronary heart disease death, nonfatal myocardial infarction, ischemic stroke, or hospitalization for unstable angina.Results: Baseline lipoprotein(a) levels (median: 21.2 mg/dl; interquartile range [IQR]: 6.7 to 59.6 mg/dl) and LDL-C [corrected for cholesterol content in lipoprotein(a)] predicted MACE. Alirocumab reduced lipoprotein(a) by 5.0 mg/dl (IQR: 0 to 13.5 mg/dl), corrected LDL-C by 51.1 mg/dl (IQR: 33.7 to 67.2 mg/dl), and reduced the risk of MACE (hazard ratio [HR]: 0.85; 95% confidence interval [CI]: 0.78 to 0.93). Alirocumab-induced reductions of lipoprotein(a) and corrected LDL-C independently predicted lower risk of MACE, after adjustment for baseline concentrations of both lipoproteins and demographic and clinical characteristics. A 1-mg/dl reduction in lipoprotein(a) with alirocumab was associated with a HR of 0.994 (95% CI: 0.990 to 0.999; p = 0.0081).Conclusions: Baseline lipoprotein(a) and corrected LDL-C levels and their reductions by alirocumab predicted the risk of MACE after recent ACS. Lipoprotein(a) lowering by alirocumab is an independent contributor to MACE reduction, which suggests that lipoprotein(a) should be an independent treatment target after ACS. (ODYSSEY Outcomes: Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab; NCT01663402). [ABSTRACT FROM AUTHOR]

The aim of our study was to examine the pathophysiology of ST depression (STD) in leads V1–V3 in the setting of inferior ST elevation myocardial infarction (iSTEMI) through the perspective of cardiac magnetic resonance (CMR). Methods: Differences in myocardial area at risk (MaR), infarct size, ejection fraction and myocardial segment involvement by CMR were compared in MITOCARE trial patients with first iSTEMI with ST elevation (STE), STD or no ST changes (NST) in V1–V3. The frontal plane projection of the inferior wall MaR in relationship to the anterior/posterior chest wall was calculated and compared between groups. Results: Fifty-six patients were included. Patients with STD (n = 38) and STE (n = 5) in V1–V3 had significantly larger mean MaR compared to NST (n = 13; 32 ± 7%LV, 36 ± 10%LV and 26 ± 6%LV, respectively; p = 0.01). STD in leads V1–V3 was associated with more apical inferior and mid inferoseptal involvement and had a larger mean frontal plane projection of MaR compared with NST (24 ± 6%LV vs. 20 ± 6%LV, p = 0.04). Conclusion: STD in V1–V3 in iSTEMI is associated with larger MaR, more extension into the inferoseptal segments and likely results from greater frontal plane projection of the MaR, leading to reciprocal changes on the electrocardiogram. [ABSTRACT FROM AUTHOR]

Objective: We aim to determine the correlation between ST-segment changes in leads V4-V6 and the extent of myocardial injury by cardiac magnetic resonance (CMR) in patients with inferior ST elevation (STE) myocardial infarction (iSTEMI).Design: Admission electrocardiogram and CMR data from the MITOCARE trial were used. Differences in mean myocardium at risk, infarct size, ejection fraction and myocardial segment involvement by CMR were compared in patients with first iSTEMI with STE, ST depression (STD) or no ST changes (NST) in V4-V6. Myocardial segment involvement was further evaluated by comparing proportion of patients in each group with ≥25% and ≥50% segment involvement.Results: Fifty-four patients were included. Patients with STE (n = 22) and STD (n = 16) in V4-V6 had significantly lower ejection fraction compared to NST (n = 16) (48% vs 48% vs 54%, p = .02). STE showed more apical, apical lateral and mid-inferolateral involvement but less basal inferior involvement than NST. STD exhibited greater basal inferoseptal involvement compared to STE. There were more patients with STE that had ≥25% and ≥50% apical lateral involvement compared with STD and NST groups. Patients with STD were more likely to have ≥25% and ≥50% basal inferoseptal involvement compared with STE and NST groups.Conclusion: Our study suggests that in iSTEMI, ST changes in the precordial leads V4-V6 correlates with greater myocardial injury and distribution of myocardium at risk. [ABSTRACT FROM AUTHOR]

Objective: Uncertainty exists concerning the relative merits of pharmacological versus mechanical coronary reperfusion in patients presenting early with ST-elevation myocardial infarction (STEMI) with extensive myocardium at risk. Accordingly, we investigated whether the extent of baseline ST-segment shift was related to the response of either reperfusion modality in patients with STEMI presenting within 3 h of symptoms.Methods: We analysed baseline ECGs from 1859 patients enrolled in the STrategic Reperfusion Early After Myocardial Infarction (STREAM) trial. The sum of ST-segment elevation (∑STE) and ST-segment deviation (∑STD) was categorised into quartiles and associations with the primary endpoint (30-day death/shock/congestive heart failure/re-myocardial infarction) for each reperfusion strategy (early fibrinolysis vs primary percutaneous coronary intervention) were explored.Results: Overall, there was a progressive rise in the 30-day primary endpoint according to quartiles of baseline ∑STE (10.3% (0-5 mm), 12.4% (5.5-8.5 mm), 12.1% (9-13.5 mm), 17.6% (> 14.0 mm), p = 0.008) and ∑STD (9.0% (0-9 mm), 13.5% (9.5-14 mm), 14.7% (14.5-20 mm), 15.3% (> 20 mm), p = 0.019). Both ∑STE and ∑STD were associated with the primary endpoint (∑STE: p = 0.071; ∑STD: p = 0.024). However, there was no interaction between quartiles of baseline ∑STE or ∑STD and efficacy of either reperfusion strategy on the 30-day clinical outcomes (∑STE: p (interaction) = 0.696; ∑STD: p (interaction) = 0.542).Conclusions: These data demonstrate an association between ∑STE or ∑STD on the baseline ECG and clinical events at 30 days following reperfusion therapy in STEMI. More importantly, the response to different reperfusion strategies was not influenced by the extent of jeopardised myocardium.Trial Registration Number: NCT00623623; Post-results. [ABSTRACT FROM AUTHOR]

Background. In patients with the metabolic syndrome, the prevalence of cardiovascular disease, disease-related morbidity and mortality are reported to be significantly higher than in a population without the metabolic syndrome. We investigated the role of metabolic syndrome and related biomarkers as predictors of infarct size in patients with their first myocardial infarction. Methods. This was a cross-sectional sub-study from the 3 months follow-up in the NORwegian Study of DIstrict treatment of ST-Elevation Myocardial Infarction (NORDISTEMI), including 152 consecutive patients, all initially treated with thrombolysis. Infarct size after 3 months was determined by late gadolinium enhanced magnetic resonance imaging, measuring ventricular infarct volume in absolute and relative terms. Results. At 3 months, 33 patients (22%) were categorized as having metabolic syndrome. There was no significant difference in median infarct size between those presenting with and without the metabolic syndrome [relative infarct volume 9.0 (4.8, 15.1) % vs. 8.3 (2.9, 13.6)%, p = 0.34]. Adjusting for possible confounders did not alter the results essentially. Circulating levels of IL-18, CRP and PAI-I activity were significantly higher in patients with the metabolic syndrome while adiponectin concentrations were significantly lower ( p ≤ 0.01 for all). None of these variables were associated with myocardial infarct size. Conclusions. No association between the presence of metabolic syndrome and related biomarkers, and the size of the myocardial infarction was apparent in this study population. [ABSTRACT FROM AUTHOR]

Objectives: The evaluation of infarct size and left ventricular function after acute myocardial infarction is important for predicting the subsequent clinical course. This assessment can be achieved by non-invasive imaging methods, but biochemical assays are frequently used as an alternative. We investigated the ability of a single measurement of cardiac troponin T (cTnT) the third morning after onset of ST-segment elevation myocardial infarction (STEMI) to predict infarct size and left ventricular ejection fraction (LVEF). Methods: The study population consisted of 103 patients with their first STEMI treated with thrombolysis. Blood samples for determination of cTnT were drawn the third morning after onset of symptoms. Infarct size and LVEF were assessed by magnetic resonance imaging 3 months later. Results: Linear regression analysis showed a strong, significant correlation between third-day cTnT and infarct size at 3 months (r = 0.84, p < 0.0001). A significant but inverse and weaker correlation was obtained between third-day cTnT and LVEF (r = –0.63, p < 0.0001). Adjusting for age, gender, infarct location and medication changed the results marginally. Conclusions: A single cTnT value the third morning after onset of STEMI predicted the final infarct size in this group of patients with their first STEMI, and might be useful for ruling out impaired LVEF. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]