Incremental value of the combined brain-cardiac CT protocol on prediction of atrial fibrillation after stroke.

Introduction: Atrial fibrillation (AF) is one of the most common causes of ischemic stroke. It is essential to target patients at highest risk of AF detected after stroke (AFDAS), who should benefit from a prolonged rhythm screening strategy. Cardiac-CT angiography (CCTA) was added to the stroke protocol used in our institution in 2018. We sought to assess, for AFDAS, the predictive value of atrial cardiopathy markers by a CCTA performed on admission for acute ischemic stroke. Patients and Methods: From November 2018 to October 2019, consecutive stroke patients with no history of AF were included. Let atrial volume (LAV), epicardial adipose tissue (EAT) attenuation and volume, and LAA characteristics were measured on CCTA. The primary endpoint was the presence of AFDAS at follow-up, diagnosed by continuous electrocardiographic monitoring, long-term external Holter monitoring during hospital stay, or implantable cardiac monitor (ICM). Results: Sixty of the 247 included patients developed AFDAS. Multivariable analysis shows independent predictors of AFDAS: age >80 years (HR 2.46; 95%CI (1.23-4.92), p = 0.011), indexed LAV >45 mL/m2 (HR 2.58; 95%CI (1.19-5.62), p = 0.017), EAT attenuation > -85HU (HR 2.16; 95%CI (1.13-4.15), p = 0.021) and LAA thrombus (HR 2.50; 95%CI (1.06-5.93), p = 0.037). Added consecutively to AFDAS prediction AS5F score (combining age and NIHSS >5), these markers had an incrementally better predictive value compared with the global Chi2 of the initial model (p = 0.001, 0.035, and 0.015 respectively). Discussion and conclusion: Adding CCTA to the acute stroke protocol to assess markers of atrial cardiopathy associated with AFDAS may help to better stratify the AF screening strategy, including the use of an ICM.

Coronary-subclavian steal syndrome causing myocardial infarction after arteriovenous fistula creation: a case report.

Coronary subclavian steal syndrome (CSSS) caused by left subclavian artery (LSA) stenosis is a rare cause of myocardial infarction in patients having coronary artery bypass grafting (CABG), and it has also been observed after an arteriovenous fistula (AVF) was made. A 79-year-old woman who had undergone CABG years earlier and an AVF creation 1 month before experienced a non-ST-elevation myocardial infarction (NSTEMI). While selective catheterization of the left internal thoracic artery graft was impossible, a computed tomography scanner showed patency of all bypasses and proximal subocclusive LSA stenosis, and the digital blood pressure measurements objectified a haemodialysis-induced distal ischaemia. LSA's angioplasty and covered stent placement were successfully performed, resulting in symptom remission. A CSSS-induced NSTEMI due to a LSA stenosis aggravated by a homolateral AVF several years after CABG has been documented only infrequently. If vascular access is required in the presence of CSSS risk factors, the contralateral upper limb should be preferred.

Acute myocardial infarction related to coronary artery embolism: A systematic cardiac and cerebral magnetic resonance imaging study.

BACKGROUND: Coronary artery embolism (CAE) is a rare, non-atherosclerotic cause of acute myocardial infarction (MI). Atrial fibrillation (AF) is the most frequent cause of CAE, and can be associated with multiple embolisms, particularly in the brain. AIMS: To characterize CAE-related myocardial injury, assess the proportion of cardiocerebral infarction and characterize brain injuries associated with dual embolism. METHODS: In this prospective study, patients with CAE-associated MI underwent (1) cardiac magnetic resonance imaging (MRI) to assess the extent of infarct transmurality and myocardial necrosis size and (2) brain MRI to assess the proportion of simultaneous cardiocerebral infarction. We screened 1401 consecutive patients with de novo acute MI from January 2019 to June 2021. CAE was diagnosed based on clinical, angiographic and diagnostic imaging criteria. RESULTS: Overall, 29/1401 patients presented with CAE (2.1%), of whom 21 underwent cardiac and cerebral MRI. Of these, nine (43%) had an ischaemic stroke, and AF was the leading cause of CAE in 14 patients (67%). Multiple CAE were common at coronary angiography (33%). Four patients (19%) had left atrial appendage thrombus - 4/9 patients (44%) with a stroke but 0/12 patients without a stroke. On cardiac MRI, the median (interquartile range) number of segments with acute infarction was 3 (0-11) in patients with stroke and 3 (1-6) in those without. Most acute ischaemic strokes (78%) were localized in the superficial sylvian territory and only 2/21 patients (10%) had stroke sequelae. CONCLUSION: MI-related to CAE was associated with infarctions of average size but multiple locations. Systematic brain MRI revealed that 33% of cases were associated with a stroke, which was generally asymptomatic. Further studies are required to better characterize the pathophysiology, clinical course and prognostic value of CAE. Moreover, optimal management strategies remain to be determined.

Coronary artery embolism and acute coronary syndrome: A critical appraisal of existing data.

The occurrence of coronary artery embolism (CE) has been associated with various clinical conditions, including aortic and mitral prosthetic heart valve implantation, atrial fibrillation (AF), dilated cardiomyopathy, neoplasia, infective endocarditis, atrial septal defect, cardiac tumors, and hypercoagulable states. CE is also a rare cause of myocardial infarction (MI), with a prevalence of about 5%, a figure probably underestimated. The purpose of this article was to determine the current state of knowledge on acute coronary syndrome (ACS) related to CE. We thus performed a comprehensive structured literature search of the MEDLINE database for articles published between 1 January 1990 and 31 December 2021. The diagnosis of CE remains difficult despite the currently used Shibata classification, which is based on major criteria, including angiographic characteristics: globular filling defects, saddle thrombi or multiple filling defects and absence of atherosclerosis in the coronary arteries. Suspected or confirmed CE requires the identification of an etiology. There are only two published series on CE, including about 50 cases each. The three main causes in these series were: 1) atrial fibrillation (73% vs 28.3%), 2) cardiomyopathy (9.4% vs 25%) and 3) malignancy (9.6% vs 15.1%). Finally, 26.3% of the MI patients with CE had no identifiable cause of CE. When anatomically possible, analyzing the thrombus after thrombectomy may help. MI due to CE requires systematic assessment of other locations, i.e. multiple coronary and extracardiac locations. Simultaneous systemic embolization to the brain (67%), limbs (25%), kidneys (25%) or spleen (4%) is frequent, occurring in approximately 25% of CE-related MI. In the setting of acute MI, CE is associated with significant morbidity and mortality. Coronary artery thromboembolism is a rare, non-atherosclerotic, cause of ACS, and prospective studies are needed to evaluate a systematic diagnostic approach and personalized therapeutic strategies.

No impact of sub-clinical coronary artery disease identified by cardiac CT scan on the recurrence of atrial fibrillation after a single ablation procedure.

BACKGROUND: Performing a cardiac CT scan before ablation provides a better understanding of the anatomical variations of the left atrium and pulmonary veins, as well as an analysis of coronary anatomy and the calcium score. The aim of the present study was to determine whether the CT characteristics of patients with unknown CAD have an impact on recurrence of AF. METHODS: This monocentric retrospective study included patients with AF who had undergone cardiac CT prior to a single ablation. RESULTS: Among the 229 patients included in the study, 70 (30.5%) presented AF recurrence between 3 and 12 months after a single ablation. The prevalence of CAD confirmed by CT coronary angiogram and the coronary calcium score were similar in the two groups. Patients with recurrent atrial fibrillation had a significantly higher LAVI evaluated by CT scan than patients without recurrence. The ROC curve determined an optimal LAVI threshold of 49 mL/m2. In multivariate analysis, the LAVI measured by CT scan was independently associated with the risk of AF recurrence. CONCLUSIONS: Our study confirms that CAD is not a predictor of AF recurrence after a single ablation, unlike the LAVI. Further studies are necessary to re-evaluate the long-term conclusions of this work.

Acute myocarditis with autoimmune features: one-year follow-up with CMR.

In this prospective study on patients with acute myocarditis (AM), we aimed to describe the new concept of AMAF (AM with autoimmune features) similar to the previously described interstitial pneumonia with autoimmune features (IPAF). IPAF has recently emerged as a new entity, and IPAF patients appear to have fewer episodes of exacerbation and better survival than patients with idiopathic pulmonary fibrosis. Consecutive patients with infarct-like CMR-confirmed AM were classified AMAF if their serologic status measured from blood sampled at presentation was positive (antinuclear antibodies (ANA) ≥ 1:320), but without meeting established classification criteria for connective tissue disease (CTD). The myocardial tissue abnormalities and their progression were assessed on cardiac magnetic resonance (CMR) within 7 days following symptom onset and at 1 year according to their seropositivity. Among the 64 AM patients included, seven presented AMAF (11%). At baseline CMR, patients with AMAF had half as much late gadolinium enhancement (LGE) as seronegative AM patients (4.41% (1.47-4.41) of myocardial volume versus 8.82% (5.88-14.71), p = 0.01, respectively). At 1-year of follow-up, persistent myocardial scarring was less frequent in AMAF patients (n = 2 (28.6%) than seronegative AM patients (n = 38 (66.7%) (p = 0.021). AMAF, diagnosed as seropositive AM without a specific autoimmune disease, is not rare and is associated with less extensive LGE in the acute phase. In addition, AMAF patients had more favorable outcomes on 12-month CMR. Prospective studies are needed to address the clinical significance of this new concept and its long-term cardiovascular impact.

More than 50% of Persistent Myocardial Scarring at One Year in "Infarct-like" Acute Myocarditis Evaluated by CMR.

BACKGROUND: Cardiac magnetic resonance (CMR) has emerged as a reference tool for the non-invasive diagnosis of myocarditis. However, its role in follow-up (FU) after the acute event is unclear. The objectives were to assess the evolution of CMR parameters between the acute phase of infarct-like myocarditis and 12 months thereafter and to identify the predictive factors of persistent myocardial scarring at one year. METHODS: All patients with infarct-like acute myocarditis confirmed by CMR were included. CMR was performed within 8 days following symptom onset, at 3 months and at one year. One-year FU included ECG, a cardiac stress test, Holter recording, biological assessments, medical history and a quality-of-life questionnaire. Patients were classified according to the presence or absence of complete recovery at one year based on the CMR evaluation. RESULTS: A total of 174 patients were included, and 147 patients had three CMR. At one year, 79 patients (54%) exhibited persistent myocardial scarring on CMR. A multivariate analysis showed that high peak troponin at the acute phase (OR: 3.0-95%CI: 1.16-7.96-p = 0.024) and the initial extent of late gadolinium enhancement (LGE) (OR: 1.1-95%CI: 1.03-1.19-p = 0.006) were independent predictors of persistent myocardial scarring. Moreover, patients with myocardial scarring on the FU CMR were more likely to have premature ventricular contractions during the cardiac stress test (25% versus 9%, p = 0.008). CONCLUSION: Less than 50% of patients with infarct-like acute myocarditis showed complete recovery at one year. Although major adverse cardiac events were rare, ventricular dysrhythmias at one year were more frequent in patients with persistent myocardial scarring.

Left Atrial Remodeling and Brain Natriuretic Peptide Levels Variation after Left Atrial Appendage Occlusion.

BACKGROUND: Few data are available about brain natriuretic peptide (BNP) variation and left atrial remodeling after the left atrial appendage occlusion (LAAO) technique. METHODS: Prospective study included all consecutive patients successfully implanted with an LAAO device. Contrast-enhanced cardiac computed tomography (CT) was performed before and 6 weeks after the procedure with reverse left atrial remodeling defined by an increase in LA volume >10%, together with blood sampling obtained before, 48 h after device implantation and at the first visit after discharge (30-45 days) for BNP measurement. RESULTS: Among the 43 patients implanted with a complete dataset, mean end-diastolic LA volume was 139 ± 64 mL and 141 ± 62 mL at baseline and during follow-up (45 ± 15 days), respectively, showing no statistical difference (p = 0.45). No thrombus was seen on the atrial side of the device. Peridevice leaks (defined as presence of dye in the LAA beyond the device) were observed in 17 patients (40%) but were trivial or mild. Reverse atrial remodeling (RAR) at 6 weeks was observed in six patients (14%). Despite no difference in BNP levels on admission, median BNP levels at 48 h were slightly increased in RAR patients when compared with controls. During FU, BNP levels were strictly identical in both groups. These results were not modified even when each RAR case was matched with two controls on age, LVEF, creatinine levels and ACE inhibitors treatment to avoid potential confounders. CONCLUSION: Our study showed that despite the fact that the LAAO technique can induce left atrial remodeling measured by a CT scan, it does not seem to impact BNP levels on the follow-up. The results need to be transposed to clinical outcomes of this expanding population in future studies.

Detection of Myocardial Infarction by Cardiac Magnetic Resonance in Embolic Stroke Related to First Diagnosed Atrial Fibrillation.

INTRODUCTION: Elevated troponin levels are found in a significant number of patients who are diagnosed with acute embolic stroke (AES) after first diagnosed atrial fibrillation (AF). These myocardial injuries, which are known as cardiocerebral infarction (CCI), are potentially caused by coronary embolism and correspond to simultaneous cardiac and cerebral embolisms. However, this severe condition remains poorly understood. In this prospective study, we aimed to investigate the prevalence and the cardiac magnetic resonance (CMR) characteristics of CCI. MATERIALS AND METHODS: Consecutive patients with first diagnosed AF hospitalized for AES in a neurovascular intensive care unit from 2019 to 2020 were included. Troponin Ic kinetic were measured <72 h, MRI and coronary angiography or CT scan were performed <7 days after admission. Patients with significant coronary lesions were excluded. RESULTS: During the study period, 1150 patients with strokes were hospitalized in the neurovascular intensive care unit (ICU). Of these patients, 955 had an ischemic stroke and 97 had a transient ischemic attack. Among the 44 patients with AES and with first diagnosed AF, 34 patients underwent CMR and CMR analysis identified 12 MI. A significant rise in troponin (>0.10 µg/L) was observed in 35% of the total population (12/34 patients). More specifically, a rise was seen in 23% of the AES without MI group, 58% of the AES with MI. In addition, coronary embolism was identified in 3 patients who underwent coronary angiography (3/12) and MI was often (30%) localized in infero-latero-medial and infero-apical segments. Most AES were localized in the superficial sylvian territory. CONCLUSION: We found a high prevalence of CMR-confirmed double embolization sites in the acute phase of an embolic stroke. Further studies are required to better characterize the pathophysiology, clinical course and prognostic value of CCI. Moreover, optimal management strategies, including antiplatelet therapy, remain to be determined.

High rate of cardiac thrombus diagnosed by adding cardiac imaging in acute stroke computed tomography protocol.

BACKGROUND: Detection of left atrial appendage thrombus (LAAt) in acute stroke patients can be improved by cardiac computed tomography using prospective electrocardiogram-gated volume acquisition, which was added to the acute stroke computed tomography protocol in our institution in 2018. AIMS: To evaluate the factors and clinical management associated with LAAt in patients with acute ischemic stroke. METHODS: We retrospectively included 324 consecutive patients with ischemic stroke from November 2018 to October 2019. Clinical data and post-stroke management were compared in LAAt and no-LAAt patients. RESULTS: Thirty-five patients (10.8%; 95%CI 7.4-14.2) had LAAt and 289 had no-LAAt. LAAt patients were significantly older (82 ± 12 vs. 74 ± 14 yo for no-LAAt, p = 0.002), predominantly female (71% vs. 45%, p = 0.004), and were more likely to have previous atrial fibrillation (63% vs. 15%, p < 0.001) and previous stroke (32% vs. 14%, p = 0.005). There was no significant difference between groups in stroke localization or severity scales at admission or at hospital discharge. After multivariable analysis, female sex (odds ratio 2.51; 95%CI 1.09-5.77, p = 0.031), previous atrial fibrillation (odds ratio 4.87; 95%CI 2.11-11.22, p < 0.001), and left atrial volume >86 ml (odds ratio 5.33; 95%CI 1.70-16.69, p = 0.004) were independently associated with LAAt. More than a third of LAAt patients (37%) received acute heparin therapy compared to 13% of no-LAAt patients (p < 0.001). Moreover, despite comparable stroke severity at admission, the mortality rate was markedly higher in the LAAt group than in the no-LAAt group (37% vs. 13%, p < 0.001). CONCLUSIONS: Cardiac computed tomography for left atrial appendage thrombus evaluation in routine acute stroke imaging protocol could be beneficial for decision-making with regard to the initiation of early anticoagulation.

A case report of an acute coronary syndrome in a 10-year-old boy with homozygous familial hypercholesterolaemia.

BACKGROUND: Familial hypercholesterolaemia is a well-known disorder, but clinical diagnoses tend to be delayed. Acute coronary syndrome may occur in childhood. CASE SUMMARY: Our patient, a young boy with homozygous familial hypercholesterolaemia, complained of persistent chest pain at rest and suffered a non-ST-elevation myocardial infarction (NSTEMI). The diagnosis of NSTEMI was made on the basis of his clinical features, dynamic electrocardiogram changes, troponin elevation, and cardiac computed tomography findings. The patient was managed surgically by intrathoracic artery (ITA) bypass graft. During post-operative follow-up, the young patient suffered from angina pectoris from unexpected and exceptional atheroma stenosis on the ITA. DISCUSSION: Familial hypercholesterolaemia needs to be identified quickly in young patients and lipid lowering therapies should be started without delay.

Relation between high levels of myeloperoxidase in the culprit artery and microvascular obstruction, infarct size and reverse remodeling in ST-elevation myocardial infarction.

MAIN OBJECTIVE: To better understand the role of myeloperoxidases (MPO) in microvascular obstruction (MO) phenomenon and infarct size (IS) using cardiac magnetic resonance (CMR) data in patients with acute myocardial infarction (AMI). METHOD: 40 consecutive patients classified according to the median level of MPO in the culprit artery. A CMR study was performed during the week following AMI and at 6 months, with late gadolinium enhancement sequences. RESULTS: Persistent MO was observed in the same proportion (50 vs. 65%, p = 0.728) between the low vs. high MPO group levels. However, the extent of the microvascular obstruction was significantly greater in the high-MPO group (6 (0-9) vs.16.5 (0-31), p = 0.027), together with a greater infarct size, and a trend towards a lower left ventricular ejection fraction (LVEF) (p = 0.054) at one week. CMR data at 6 months showed that reverse systolic remodeling was two fold more present in the low-MPO group (p = 0.058). Interestingly, the extent of MO (8.5 (6.5-31) vs. 4.1 (3-11.55), p = 0.042) and IS remained significantly greater (24.5 (9.75-35) vs. 7.5 (2.5-18.75), p = 0.022) in the high-MPO group. Moreover, MPO in the culprit artery appeared to correlate positively with MPO in non-culprit arteries and serum, and with troponin levels and peak CK. CONCLUSION: This patient-based study revealed in patients after AMI that high MPO levels in the culprit artery were associated with more severe microvascular obstruction and greater IS. These findings may provide new insights pathophysiology explanation for the adverse prognostic impact of MO.

Incremental predictive value of mean platelet volume/platelet count ratio in in-hospital stroke after acute myocardial infarction.

Stroke is a serious complication after acute myocardial infarction (AMI) and is associated with an increased risk of death. Though the pathophysiological mechanisms are not exactly known, increased inflammation and platelet reactivity could play an important role in the occurrence of stroke during AMI. We aimed to investigate the relationship between both mean platelet volume (MPV), a parameter of platelet function, and C-reactive protein (CRP) and the occurrence of in-hospital ischemic stroke (IHS) after AMI. Data were obtained from a French regional survey for AMI that included 5976 patients admitted to an intensive care unit (ICU) between 2001 and 2010. Patients were divided into two groups according to the occurrence of IHS. MPV, platelet count (PC), and CRP were routinely measured at admission to the ICU; 99 (1.6%) IHSs were recorded during hospitalization after admission for AMI. In multivariate analysis, IHS was independently associated with a history of stroke (OR: 1.99%, CI: 1.1-3.49, p = 0.01), impaired left ventricular ejection fraction <40% (OR: 1.88, 95% CI: 1.20-2.94, p = 0.006), impaired renal function (OR: 1.94, 95% CI: 1.27-2.95, p = 0.002), CRP > 10 mg/l (OR: 2.19, 95% CI: 1.44-3.33, p < 0.001), and MPV/PC ratio (OR: 1.04, 95% CI: 1.01-1.08, p = 0.023). Compared with the first to fourth quintiles, the last quintile of the MPV/PC ratio was associated with higher rates of IHS on survival curve analysis (p = 0.014). At hospital admission, a high MPV/PC ratio and a high level of CRP might help to identify patients at increased risk of IHS. Moreover, these results provide new insights into the potential role played by increased inflammation and platelet reactivity in the occurrence of stroke after AMI.