NT-proBNP level before primary PCI and risk of poor myocardial reperfusion: Insight from the On-TIME II trial.

BACKGROUND: N-terminal fragment of the brain natriuretic peptide prohormone (NT-proBNP), a marker for neurohumoral activation, has been associated with adverse outcome in patients with myocardial infarction. NT-proBNP levels may reflect extensive ischemia and microvascular damage, therefore we investigated the potential association between baseline NT-proBNP level and ST-resolution (STR), a marker of myocardial reperfusion, after primary percutaneous coronary intervention (pPCI). METHODS: we performed a post-hoc analysis of the On-TIME II trial (which randomized ST-elevation myocardial infarction (STEMI) patients to pre-hospital tirofiban administration vs placebo). Patients with measured NT-proBNP before angiography were included. Multivariate logistic-regression analyses was performed to investigate the association between baseline NTproBNP level and STR one hour after pPCI. RESULTS: Out of 984 STEMI patients, 918 (93.3%) had NT-proBNP values at baseline. Patients with STR <70% had higher NT-proBNP values compared to patients with complete STR (>70%) [Mean ±SD 375.2 ±1021.7 vs 1007.4 ±2842.3, Median (IQR) 111.7 (58.4-280.0) vs 168.0 (62.3-601.3), P <.001]. At multivariate logistic regression analysis, independent predictors associated with higher risk of poor myocardial reperfusion (STR <70%) were: NT-proBNP (OR 1.17, 95%CI 1.04-1.31, P = .009), diabetes mellitus (OR 1.87, 95%CI 1.14-3.07, P = .013), anterior infarct location (OR 2.74, 95% CI 2.00-3.77, P <.001), time to intervention (OR 1.06, 95%CI 1.01-1.11, P = .021), randomisation to placebo (OR 1.45, 95%CI 1.05-1.99, P = .022). CONCLUSIONS: In STEMI patients, higher baseline NT-proBNP level was independently associate with higher risk of poor myocardial reperfusion, supporting the potential use of NT-proBNP as an early marker for risk stratification of myocardial reperfusion after pPCI in STEMI patients.

Value of the platelet-to-lymphocyte ratio in the prediction of left ventricular thrombus in anterior ST-elevation myocardial infarction with left ventricular dysfunction.

BACKGROUND: The predictors of left ventricular thrombus (LVT) formation are not well defined in the contemporary era, especially in those patients at high risk. We aimed to evaluate whether the platelet/lymphocyte ratio (PLR) is valuable in the determination of LVT formation in patients with anterior ST-elevation myocardial infarction (STEMI) and left ventricular (LV) dysfunction. METHODS: The LVT group (n = 46) was identified from anterior STEMI patients with LV dysfunction who were treated with primary percutaneous coronary intervention (PCI) from January 2017 to December 2019 at the China-Japan Union Hospital of Jilin University. The no-LVT group (n = 92) were also selected from the same batch of patients and were age- and sex-matched to the patients with LVT. The PLR was determined at admission and was calculated as the ratio of the platelet count to the lymphocyte count using the complete blood count. The presence of LVT was determined by echocardiography. RESULTS: The PLR were significantly higher in patients with LVT than in no-LVT group (p = 0.001). In a receiver operator characteristic curve (ROC) analysis, using a cut-off value of 118.07 (AUC 0.673, 95% CI: 0.574-0.771, P = 0.001), the PLR could independently predict the occurrence of LVT. Multivariate analysis showed that an increased PLR (OR = 1.011, 95% CI: 1.004-1.018, P = 0.002), the presence of a left ventricular aneurysm (OR = 46.350, 95% CI: 5.659-379.615, P < 0.001) and increased DTBT (OR = 1.005, 95% CI: 1.001-1.009, P = 0.012) were independent predictors of LVT formation. CONCLUSIONS: In acute anterior STEMI patients with LV dysfunction, an increased PLR and DTBT and the presence of an LV aneurysm were independent predictors of LVT formation. A larger prospective study is warranted to evaluate this result. TRIAL REGISTRATION: This study was registered (May 4, 2019) on Chinese Clinical Trial Registry ( ChiCTR-DDD-17011214 ).

Heart Failure Stimulates Tumor Growth by Circulating Factors.

BACKGROUND: Heart failure (HF) survival has improved, and nowadays, many patients with HF die of noncardiac causes, including cancer. Our aim was to investigate whether a causal relationship exists between HF and the development of cancer. METHODS: HF was induced by inflicting large anterior myocardial infarction in APCmin mice, which are prone to developing precancerous intestinal tumors, and tumor growth was measured. In addition, to rule out hemodynamic impairment, a heterotopic heart transplantation model was used in which an infarcted or sham-operated heart was transplanted into a recipient mouse while the native heart was left in situ. After 6 weeks, tumor number, volume, and proliferation were quantified. Candidate secreted proteins were selected because they were previously associated both with (colon) tumor growth and with myocardial production in post-myocardial infarction proteomic studies. Myocardial gene expression levels of these selected candidates were analyzed, as well as their proliferative effects on HT-29 (colon cancer) cells. We validated these candidates by measuring them in plasma of healthy subjects and patients with HF. Finally, we associated the relation between cardiac specific and inflammatory biomarkers and new-onset cancer in a large, prospective general population cohort. RESULTS: The presence of failing hearts, both native and heterotopically transplanted, resulted in significantly increased intestinal tumor load of 2.4-fold in APCmin mice (all P<0.0001). The severity of left ventricular dysfunction and fibrotic scar strongly correlated with tumor growth ( P=0.002 and P=0.016, respectively). We identified several proteins (including serpinA3 and A1, fibronectin, ceruloplasmin, and paraoxonase 1) that were elevated in human patients with chronic HF (n=101) compared with healthy subjects (n=180; P<0.001). Functionally, serpinA3 resulted in marked proliferation effects in human colon cancer (HT-29) cells, associated with Akt-S6 phosphorylation. Finally, elevated cardiac and inflammation biomarkers in apparently healthy humans (n=8319) were predictive of new-onset cancer (n=1124) independently of risk factors for cancer (age, smoking status, and body mass index). CONCLUSIONS: We demonstrate that the presence of HF is associated with enhanced tumor growth and that this is independent of hemodynamic impairment and could be caused by cardiac excreted factors. A diagnosis of HF may therefore be considered a risk factor for incident cancer.

Incidence and Significance of Spontaneous ST Segment Re-elevation After Reperfused Anterior Acute Myocardial Infarction　- Relationship With Infarct Size, Adverse Remodeling, and Events at 1 Year.

BACKGROUND: Up to 25% of patients with ST elevation myocardial infarction (STEMI) have ST segment re-elevation after initial regression post-reperfusion and there are few data regarding its prognostic significance.Methods and Results:A standard 12-lead electrocardiogram (ECG) was recorded in 662 patients with anterior STEMI referred for primary percutaneous coronary intervention (PPCI). ECGs were recorded 60-90 min after PPCI and at discharge. ST segment re-elevation was defined as a ≥0.1-mV increase in STMax between the post-PPCI and discharge ECGs. Infarct size (assessed as creatine kinase [CK] peak), echocardiography at baseline and follow-up, and all-cause death and heart failure events at 1 year were assessed. In all, 128 patients (19%) had ST segment re-elevation. There was no difference between patients with and without re-elevation in infarct size (CK peak [mean±SD] 4,231±2,656 vs. 3,993±2,819 IU/L; P=0.402), left ventricular (LV) ejection fraction (50.7±11.6% vs. 52.2±10.8%; P=0.186), LV adverse remodeling (20.1±38.9% vs. 18.3±30.9%; P=0.631), or all-cause mortality and heart failure events (22 [19.8%] vs. 106 [19.2%]; P=0.887) at 1 year. CONCLUSIONS: Among anterior STEMI patients treated by PPCI, ST segment re-elevation was present in 19% and was not associated with increased infarct size or major adverse events at 1 year.

Association of serum cystatin C levels with myocardial perfusion and cardiac functional recovery in patients with anterior wall ST elevation myocardial infarction treated with primary coronary intervention.

This study sought to investigate the association of baseline serum cystatin C levels with myocardial perfusion and cardiac functional recovery in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). 108 patients with a first anterior STEMI who underwent PPCI were enrolled. Serum cystatin C was measured by immunoturbidimetric method. Patients were divided into two groups according to the median cystatin C levels on admission: group 1 (≥median, n = 54) and group 2 (

Left ventricular apical aneurysm following primary percutaneous coronary intervention.

Left ventricular apical aneurysm (LVAA) is a serious complication of acute anterior myocardial infarction (MI). The purpose of our study was to investigate the clinical features of LVAA in the primary PCI era. A total of 161 acute anterior MI patients who had primary PCI and had an echocardiogram on chronic phase were included. The development of LVAA was reviewed on chronic phase. Univariate and multivariate logistic regression analyses were performed to identify the predictors of LVAA. Primary stenting was performed in 160 patients (99.4 %). Procedural success was obtained in all patients with a final TIMI flow grade 3 obtained in 142 patients (88.2 %). LVAA developed in the chronic phase in 29 patients (18.0 %). Multivariate logistic regression analysis revealed that peak CK (500 mU/ml increase; OR 1.24, 95 % CI 1.09-1.41, p = 0.001), heart rate at discharge (5/min increase; OR 1.39, 95 % CI 1.03-1.87, p = 0.03), final TIMI flow grade ≤2 (vs. TIMI 3; OR 6.95, 95 % CI 1.70-28.36, p = 0.01) and final myocardial brush grade (MBG) ≤2 (vs. MBG 3; OR 4.33, 95 % CI 1.06-17.66, p = 0.04) were significantly associated with the development of LVAA. The initial TIMI flow grade or the grade of collateral flow was not associated with LVAA. In conclusion, peak CK, heart rate, and final TIMI flow grade or final MBG ≤2 were significantly associated with the development of LVAA. Achieving a TIMI flow grade 3 by primary PCI may be important for preventing LVAA.

[Myocardial infarction associated with oral contraceptive use, smoking and elevated cholesterol level in a young patient]. / Fiatalkorban lezajlott myocardialis infarctus összefüggése a hormonális fogamzásgátló szedésével, a dohányzással és az emelkedett koleszterinszinttel.

Oral hormonal contraceptives are the safest methods for young patients to avoid unwanted pregnancy. They are well accepted and have certain beneficial effects; however, physicians should pay attention to risk factors even when applied in young age. Obesity, dyslipidemia, smoking and oral contraceptive pills alone or in combination may lead to serious adverse events. Authors present a young woman who developed acute myocardial infarction in association with several unconsidered risk factors including the use of contraceptive pills.

In-hospital prognostic value of admission plasma B-type natriuretic peptide levels in patients undergoing primary angioplasty for acute ST-elevation myocardial infarction.

OBJECTIVES: We assessed in-hospital prognostic value of admission plasma B-type natriuretic peptide (BNP) levels in patients undergoing primary percutaneous coronary intervention (p-PCI) for acute ST-elevation myocardial infarction (STEMI). STUDY DESIGN: In a retrospective design, we evaluated 992 patients (801 males, 191 females; mean age 56 ± 12 years) treated with p-PCI for STEMI. The patients were divided into two groups according to the admission BNP levels, taking the cut-off value of BNP as 100 pg/ml; i.e, ≥ 100 pg/ml (n=334, 33.7%) and <100 pg/ml (n=658, 66.3%). Postprocedural angiographic and clinical in-hospital results were recorded. RESULTS: No-reflow (24% vs. 9%), heart failure (32.3% vs. 5.5%) and death (15.6% vs. 1.7%) were significantly more common in patients with BNP ≥ 100 pg/ml (p<0.001). In multivariate analysis, elevated baseline BNP level was identified as an independent predictor of no-reflow (OR=1.83; 95% CI 1.22-2.74, p=0.003), acute heart failure (OR=2.67; 95% CI 1.55-4.58, p<0.001), and in-hospital mortality (OR=3.28; 95% CI 1.51-7.14, p=0.003). In receiver operating characteristic curve analysis, the area under the curve and sensitivity/specificity of the cut-off value of BNP (100 pg/ml) for prediction of clinical endpoints were 0.741 and 58.6%/70.3% for no-reflow, 0.822 and 75%/73.3% for heart failure, and 0.833 and 82.5%/69.4% for death, respectively (p<0.001 for all). CONCLUSION: Elevated admission BNP level is an independent predictor of angiographic no-reflow, acute heart failure, and mortality in STEMI patients during in-hospital period, suggesting that it might be incorporated into traditional risk scoring systems to improve early risk stratification.

Type 2 myocardial infarction and myocardial injury: eligibility for novel medical therapy to derisk clinical trials.

BACKGROUND: Patients with type 2 myocardial infarction (T2MI) and other mechanisms of nonthrombotic myocardial injury have an unmet therapeutic need. Eligibility for novel medical therapy is generally uncertain. METHODS: We predefined colchicine, eplerenone and ticagrelor as candidates for repurposing towards novel therapy for T2MI or myocardial injury. Considering eligibility for randomisation in a clinical trial, each drug was classified according to indications and contraindications for therapy and survival for at least 24 hours following admission. Eligibility criteria for prescription were evaluated against the Summary of Medical Product Characteristics. Consecutive hospital admissions were screened to identify patients with ≥1 high-sensitivity troponin-I value >99th percentile. Endotypes of myocardial injury were adjudicated according to the Fourth Universal Definition of MI. Patients' characteristics and medication were prospectively evaluated. RESULTS: During 1 March to 15 April 2020, 390 patients had a troponin I>URL. Reasons for exclusion: type 1 MI n=115, indeterminate diagnosis n=42, lack of capacity n=14, death <24 hours n=7, duplicates n=2. Therefore, 210 patients with T2MI/myocardial injury and 174 (82.8%) who survived to discharge were adjudicated for treatment eligibility. Patients who fulfilled eligibility criteria initially on admission and then at discharge were colchicine 25/210 (11.9%) and 23/174 (13.2%); eplerenone 57/210 (27.1%) and 45/174 (25.9%); ticagrelor 122/210 (58.1%) and 98/174 (56.3%). Forty-six (21.9%) and 38 (21.8%) patients were potentially eligible for all three drugs on admission and discharge, respectively. CONCLUSION: A reasonably high proportion of patients may be considered eligible for repurposing novel medical therapy in secondary prevention trials of type 2 MI/myocardial injury.

Effect of human peripheral monocyte subsets on coronary flow reserve in infarct-related artery in patients with primary anterior acute myocardial infarction.

1. In the present study, we investigated the relationships between relative levels of specific peripheral monocyte subsets and coronary flow velocity reserve (CFVR) during the subacute phase in patients with acute myocardial infarction (AMI). 2. The study was performed on 29 patients with primary anterior AMI who had been successfully treated using primary percutaneous coronary intervention. Two monocyte subsets (CD14(+)CD16(-) and CD14(+)CD16(+)) were measured by flow cytometry. Transthoracic Doppler echocardiography was used to measure CFVR on Days 4 and 7 after the onset of AMI onset. We defined DeltaCFVR as the difference in CFVR values between Days 4 and 7. The extent of myocardial salvage on Day 7 after AMI was evaluated by cardiovascular magnetic resonance (CMR) imaging as the difference between the area of myocardium at risk and the area of necrotic myocardium. 3. There was a significant negative correlation between DeltaCFVR and peak CD14(+)CD16(-) monocyte counts in AMI patients, whereas no significant association was found between CD14(+)CD16(+) monocyte counts and DeltaCFVR. There was a significant positive correlation between DeltaCFVR and the extent of myocardial salvage. 4. In conclusion, peak levels of CD14(+)CD16(-) monocytes following primary anterior AMI were closely related to the extent of microvascular injury.

Diminished Reactive Hematopoiesis and Cardiac Inflammation in a Mouse Model of Recurrent Myocardial Infarction.

BACKGROUND: Recurrent myocardial infarction (MI) is common in patients with coronary artery disease and is associated with high mortality. Long-term reprogramming of myeloid progenitors occurs in response to inflammatory stimuli and alters the organism's response to secondary inflammatory challenges. OBJECTIVES: This study examined the effect of recurrent MI on bone marrow response and cardiac inflammation. METHODS: The investigators developed a surgical mouse model in which 2 subsequent MIs affected different left ventricular regions in the same mouse. Recurrent MI was induced by ligating the left circumflex artery followed by the left anterior descending coronary artery branch. The study characterized the resulting ischemia by whole-heart fluorescent coronary angiography after optical organ clearing and by cardiac magnetic resonance imaging. RESULTS: A first MI-induced bone marrow "memory" via a circulating signal, reducing hematopoietic maintenance factor expression in bone marrow macrophages. This dampened the organism's reaction to subsequent events. Despite a similar extent of injury according to troponin levels, recurrent MI caused reduced emergency hematopoiesis and less leukocytosis than a first MI. Consequently, fewer leukocytes migrated to the ischemic myocardium. The hematopoietic response to lipopolysaccharide was also mitigated after a previous MI. The increase of white blood count in 28 patients was lower after recurrent MI compared with their first MI. CONCLUSIONS: The data suggested that hematopoietic and innate immune responses are shaped by a preceding MI.

Relationship between apical thrombus formation and blood viscosity in acute anterior myocardial infarction patients.

Aim: This study sought to investigate the predictive value of whole blood viscosity (WBV) to identify high-risk patients who will develop an apical thrombus during the acute phase of anterior transmural infarction. Materials & methods: Consecutive 1726 patients with first acute anterior myocardial infarction were evaluated. WBV was calculated according to the Simone's formula. Results: Patients with an apical thrombus had prolonged pain to balloon time, higher rate of post-PCI thrombolysis in myocardial infarction flow ≤1 and significantly higher mean WBV values at both shear rates than those without an apical thrombus. Conclusion: WBV values at both shear rates were found to be significant and independent predictors for early LV apical thrombus formation complicating a first-ever anterior wall myocardial infarction.

Association Between C-Reactive Protein to Albumin Ratio and Left Ventricular Thrombus Formation Following Acute Anterior Myocardial Infarction.

Left ventricular thrombus (LVT) is associated with inflammatory response in survivors with anterior ST-elevation myocardial infarction (STEMI). The C-reactive protein to albumin ratio (CAR) has been proposed as a marker of inflammation. However, there is a lack of data with respect to the role of CAR in LVT development. We investigated the relationship between CAR and LVT development in patients with anterior STEMI treated percutaneously; 955 consecutive patients were enrolled and LVT was observed in 126 (13.2%) patients. Clinical, demographic, and laboratory parameters were recorded. The CAR was significantly higher in patients with LVT (12.6 [8.6-16.1] vs 18.1 [11.5-23], P < .001). Other independent predictors for LVT development were lower ejection fraction, the presence of left ventricular apical aneurysm, proximal left anterior descending lesion location, glycoprotein IIb/IIIa inhibitors treatment, >1 diseased arteries, higher total protein level, neutrophil count, and peak creatine kinase myocardial band activity. In conclusion, the CAR may be useful as a simple tool for predicting LVT development among survivors of anterior STEMI.

Ischemic changes in lead aVR is associated with left ventricular thrombus or high-grade spontaneous echocontrast in patients with acute anterior myocardial infarction.

OBJECTIVE: The aim of this study was to investigate the relationship between ischemic changes in the lead aVR and left ventricular thrombus (LVT) or high-grade spontaneous echo contrast (SEC) in patients with acute anterior myocardial infarction (MI). METHODS: Quantitative T wave polarity in lead aVR (TPaVR) and ST segment deviation in the lead aVR (STaVR) measured from a surface electrocardiogram (ECG), as well as the absolute numerical values, were recorded. The ST/TPaVR ratio was obtained by dividing the larger absolute value by the smaller. The presence of LVT or high-grade SEC was recorded using echocardiograpy. The SYNTAX score (SS), clinical SS (cSS), and residual SS (rSS) were calculated from angiography results. RESULTS: A total of 34 patients with LVT or high-grade SEC were included in Group 1. Group 2 comprised 170 patients who did not have any LVT or high-grade SEC. The P wave duration, V2 ST-segment elevation, TPaVR, cSS, and ST/TPaVR ratio were significantly higher in Group 1. The ejection fraction (EF) and STaVR were significantly higher in Group 2. The EF (Odds ratio [OR]: 0.9, 95% confidence interval [CI]: 0.833-0.973; p=0.008), TPaVR (OR: 1.454, 95% CI: 1.074-1.967; p=0.015), and ST/TPaVR ratio (OR: 1.6, 95% CI: 1.307-1.959; p<0.001) were determined to be independent predictors for Group 1. CONCLUSION: Ischemic changes in the lead aVR are closely associated with LVT or high-grade SEC in anterior MI patients.

Echocardiographic diastolic function evolution in patients with an anterior Q-wave myocardial infarction: insights from the REVE-2 study.

AIMS: Myocardial fibrosis plays a key role in the development of adverse left ventricular remodelling after myocardial infarction (MI). This study aimed to determine whether the circulating levels of BNP, collagen peptides, and galectin-3 are associated with diastolic function evolution (both deterioration and improvement) at 1 year after an anterior MI. METHODS AND RESULTS: The REVE-2 is a prospective multicentre study including 246 patients with a first anterior Q-wave MI. Echocardiographic assessment was performed at hospital discharge and ±1 year after MI. BNP, galectin-3, and collagen peptides were measured ±1 month after MI. Left ventricular diastolic dysfunction (DD) was defined according to the presence of at least two criteria of echocardiographic parameters: septal e' < 8 cm/s, lateral e' < 10 cm/s, and left atrial volume ≥ 34 mL/m2 . At baseline, 87 (35.4%) patients had normal diastolic function and 159 (64.6%) patients had DD. Follow-up of 61 patients among the 87 patients with normal diastolic function at baseline showed that 22 patients (36%) developed DD at 1 year post-MI. The circulating levels of amino-terminal propeptide of type III procollagen > 6 mg/L [odds ratio (OR) = 5.29; 95% confidence interval (CI) = 1.05-26.66; P = 0.044], galectin-3 > 13 µg/L (OR = 5.99; 95% CI = 1.18-30.45; P = 0.031), and BNP > 82 ng/L (OR = 10.25; 95% CI = 2.36-44.50; P = 0.002) quantified at 1 month post-MI were independently associated with 1 year DD. Follow-up of the 137 patients with DD at baseline among the 159 patients showed that 36 patients (26%) had a normalized diastolic function at 1 year post-MI. Patients with a BNP > 82 ng/L were less likely to improve diastolic function (OR = 0.06; 95% CI = 0.01-0.28; P = 0.0003). CONCLUSIONS: The present study suggests that circulating levels of amino-terminal propeptide of type III procollagen, galectin-3, and BNP may be independently associated with new-onset DD in post-MI patients.

Predictors of Left Ventricular Remodeling After Myocardial Infarction in Patients With a Patent Infarct Related Coronary Artery After Percutaneous Coronary Intervention (from the Post-Myocardial Infarction Remodeling Prevention Therapy [PRomPT] Trial).

Left ventricular (LV) remodeling after myocardial infarction (MI) is a strong predictor of heart failure and mortality. The predictors of long-term remodeling after MI have been incompletely studied. We therefore examined the correlates of LV remodeling in patients with large ST-segment elevation myocardial infarction and a patent infarct artery after percutaneous 2coronary intervention (PCI) from the randomized Post-Myocardial Infarction Remodeling Prevention Therapy trial. Peri-infarct pacing had a neutral effect on long-term remodeling in patients with large first MI. The present analysis includes 109 patients in whom an open artery was restored after PCI, and in whom LV end-diastolic volume (LVEDV) at baseline and 18 months was assessed by transthoracic echocardiography. Multivariable models were fit to identify the independent predictors of LVEDV at baseline and 18 months. By multivariable analysis, male sex (p = 0.004) and anterior MI location (p = 0.03) were independently associated with baseline LVEDV. The following variables were independent predictors of increased LVEDV at 18 months: younger age (p = 0.01), male sex (p = 0.03), peak creatine phosphokinase (p = 0.03), shorter time from MI to baseline transthoracic echocardiography (p = 0.04), baseline LVEDV (p < 0.0001), and lack of statin use (p = 0.03). In conclusion, patients with large MI and an open infarct artery after PCI, anterior MI location, and male sex were associated with greater baseline LVEDV, but MI location was not associated with 18-month LVEDV. In contrast, younger age, peak creatine phosphokinase, male sex, baseline LVEDV, and lack of statin use were associated with long-term LV remodeling.

[Ischemic stroke related to spontaneous]. / Accident vasculaire cérébral ischémique en rapport avec hématome coronaire spontané.

Cardiovascular disease in women is a particularly complex pathology especially in the youngest population. The clinical presentation of acute coronary syndromes is sometimes misleading and does not necessarily point to the potential presence of cardiac disease given the frequent absence of cardiovascular risks. Such complexity results in delayed diagnosis, which worsens the outcome of myocardial infarction and generates complications related to the absence of coronary revascularization. We report the case of a patient who suffered an (undiagnosed) apical myocardial infarction that went undetected and was complicated by a voluminous intraventricular thrombus with embolus migration in the cerebral circulation resulting in an ischemic accident. The combination of these two pathologies make their therapeutic management particularly difficult. As widely reported in the literature, the outcome of myocardial infarction in women is poorer than in their male counterparts for a number of reasons. We can assume that in the youngest patients, another physiopathological mechanism is often involved, namely, the occurrence of hematoma and spontaneous coronary dissection. Diagnosis is often difficult even with coronary angiography diagnosis. As shown in the case reported here, initial examination results, if not thoroughly analyzed, may be erroneously interpreted as normal. It is also likely that the presence of hematoma or coronary wall dissection without any plaque rupture may negatively influence the outcome owing to the implementation of inappropriate treatments. In conclusion, in patients presenting with an ischemic cerebral accident, meticulous cardiac examination must be performed even in young women with no cardiovascular risk factors given that the occurrence of hematoma or coronary dissection may contribute to the formation of mural thrombi in the setting of myocardial infarction. Cardiac MRI seems to be particularly effective in the diagnosis of myocardial infarction complicated by the presence of intracavitary thrombi.

Localised pericardial effusion mimicking anterior myocardial infarction following coronary angiography.

The diagnosis of pericarditis is important, especially in patients assumed to have acute coronary syndrome. Distinguishing these two conditions is vital but not always easy. Accurate diagnosis is essential to provide appropriate treatment as soon as possible and to avoid inappropriate invasive procedures. By highlighting this distinction, we report a case of pericarditis that occurred after percutaneous coronary intervention and mimicked acute coronary syndrome.

The predictive value of M30 and oxidative stress for left ventricular remodeling in patients with anterior ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention.

BACKGROUND: Left ventricular (LV) remodeling is an important pathophysiological event that develops following acute myocardial infarction and causes LV systolic dysfunction. Mechanisms such as apoptosis, necrosis, and oxidative stress play an important role in LV remodeling. OBJECTIVES: This study aimed to determine the relationship between the development of LV remodeling and the apoptosis marker M30 in patients with anterior ST-segment elevation myocardial infarction (STEMI) who were treated with primary percutaneous coronary intervention (PCI). MATERIALS AND METHODS: This retrospective study included 255 consecutive patients (210 men, 45 women, mean age 54.9±11.8 years) with anterior STEMI who were treated with primary PCI. Blood samples were obtained from each patient at admission and 24 h after admission for measurements of M30, M65, oxidative parameters, and biochemical parameters. Transthoracic echocardiography was performed in each patient within 24 h of infarction and 6 months after infarction. LV remodeling was defined as greater than or equal to 20% increase in end-diastolic volume 6 months after primary PCI. The patients were divided into two groups on the basis of 6 months of post-primary PCI follow-up findings: LV remodeling group and non-LV remodeling group. RESULTS: In all, 60 patients received LV remodeling and 195 did not receive LV remodeling at 6 months after primary PCI. Total oxidative stress, M30 and M65 levels, and the oxidative stress index were significantly higher and the total antioxidant capacity and M65/M30 ratio were lower in the LV remodeling group (P<0.05, for all). Brain natriuretic peptide, M30, and oxidative stress index were independent predictors of LV remodeling (P<0.05 for all). Receiver operating characteristic curve analysis showed that the M30 cut-off value for predicting LV remodeling was 144.9 U/l (80% sensitivity and 77% specificity, P<0.001). CONCLUSION: In patients with anterior STEMI treated with primary PCI, the apoptosis marker M30 might be useful for predicting LV remodeling and subsequent LV systolic dysfunction.

Relation of Left Ventricular Mass and Infarct Size in Anterior Wall ST-Segment Elevation Acute Myocardial Infarction (from the EMBRACE STEMI Clinical Trial).

Biomarker measures of infarct size and myocardial salvage index (MSI) are important surrogate measures of clinical outcomes after a myocardial infarction. However, there is variability in infarct size unaccounted for by conventional adjustment factors. This post hoc analysis of Evaluation of Myocardial Effects of Bendavia for Reducing Reperfusion Injury in Patients With Acute Coronary Events (EMBRACE) ST-Segment Elevation Myocardial Infarction (STEMI) trial evaluates the association between left ventricular (LV) mass and infarct size as assessed by areas under the curve for creatine kinase-MB (CK-MB) and troponin I release over the first 72 hours (CK-MB area under the curve [AUC] and troponin I [TnI] AUC) and the MSI. Patients with first anterior STEMI, occluded left anterior descending artery, and available LV mass measurement in EMBRACE STEMI trial were included (n = 100) (ClinicalTrials.govNCT01572909). MSI, end-diastolic LV mass on day 4 cardiac magnetic resonance, and CK-MB and troponin I concentrations were evaluated by a core laboratory. After saturated multivariate analysis, dominance analysis was performed to estimate the contribution of each independent variable to the predicted variance of each outcome. In multivariate models that included age, gender, body surface area, lesion location, smoking, and ischemia time, LV mass remained independently associated with biomarker measures of infarct size (CK-MB AUC p = 0.02, TnI AUC p = 0.03) and MSI (p = 0.003). Dominance analysis demonstrated that LV mass accounted for 58%, 47%, and 60% of the predicted variances for CK-MB AUC, TnI AUC, and MSI, respectively. In conclusion, LV mass accounts for approximately half of the predicted variance in biomarker measures of infarct size. It should be considered as an adjustment variable in studies evaluating infarct size.