Beta-Blockers after Myocardial Infarction and Preserved Ejection Fraction.

BACKGROUND: Most trials that have shown a benefit of beta-blocker treatment after myocardial infarction included patients with large myocardial infarctions and were conducted in an era before modern biomarker-based diagnosis of myocardial infarction and treatment with percutaneous coronary intervention, antithrombotic agents, high-intensity statins, and renin-angiotensin-aldosterone system antagonists. METHODS: In a parallel-group, open-label trial performed at 45 centers in Sweden, Estonia, and New Zealand, we randomly assigned patients with an acute myocardial infarction who had undergone coronary angiography and had a left ventricular ejection fraction of at least 50% to receive either long-term treatment with a beta-blocker (metoprolol or bisoprolol) or no beta-blocker treatment. The primary end point was a composite of death from any cause or new myocardial infarction. RESULTS: From September 2017 through May 2023, a total of 5020 patients were enrolled (95.4% of whom were from Sweden). The median follow-up was 3.5 years (interquartile range, 2.2 to 4.7). A primary end-point event occurred in 199 of 2508 patients (7.9%) in the beta-blocker group and in 208 of 2512 patients (8.3%) in the no-beta-blocker group (hazard ratio, 0.96; 95% confidence interval, 0.79 to 1.16; P = 0.64). Beta-blocker treatment did not appear to lead to a lower cumulative incidence of the secondary end points (death from any cause, 3.9% in the beta-blocker group and 4.1% in the no-beta-blocker group; death from cardiovascular causes, 1.5% and 1.3%, respectively; myocardial infarction, 4.5% and 4.7%; hospitalization for atrial fibrillation, 1.1% and 1.4%; and hospitalization for heart failure, 0.8% and 0.9%). With regard to safety end points, hospitalization for bradycardia, second- or third-degree atrioventricular block, hypotension, syncope, or implantation of a pacemaker occurred in 3.4% of the patients in the beta-blocker group and in 3.2% of those in the no-beta-blocker group; hospitalization for asthma or chronic obstructive pulmonary disease in 0.6% and 0.6%, respectively; and hospitalization for stroke in 1.4% and 1.8%. CONCLUSIONS: Among patients with acute myocardial infarction who underwent early coronary angiography and had a preserved left ventricular ejection fraction (≥50%), long-term beta-blocker treatment did not lead to a lower risk of the composite primary end point of death from any cause or new myocardial infarction than no beta-blocker use. (Funded by the Swedish Research Council and others; REDUCE-AMI ClinicalTrials.gov number, NCT03278509.).

Prepercutaneous coronary intervention Zalunfiban dose-response relationship to target vessel blood flow at initial angiogram in st-elevation myocardial infarction - A post hoc analysis of the cel-02 phase IIa study.

BACKGROUND: Zalunfiban (RUC-4) is a novel, subcutaneously administered glycoprotein IIb/IIIa inhibitor (GPI) designed for prehospital treatment to initiate reperfusion in the infarct-related artery (IRA) before primary percutaneous coronary intervention in patients with ST-elevation myocardial infarction (STEMI). Since GPIs have been reported to rapidly reperfuse IRAs, we assessed whether there was a dose-dependent relationship between zalunfiban treatment and angiographic reperfusion indices and thrombus grade of the IRA at initial angiogram in patients with STEMI. METHODS: This was a post hoc analysis from the open-label Phase IIa study that investigated the pharmacodynamics, pharmacokinetics, and tolerability of three doses of zalunfiban - 0.075, 0.090 and 0.110 mg/kg - in STEMI patients. This analysis explored dose-dependent associations between zalunfiban and three angiographic indices of the IRA, namely coronary and myocardial blood flow and thrombus burden. Zalunfiban was administered in the cardiac catheterization laboratory prior to vascular access, ∼10 to 15 minutes before the initial angiogram. All angiographic data were analyzed by a blinded, independent, core laboratory. RESULTS: Twentyfour out of 27 STEMI patients were evaluable for angiographic analysis (0.075 mg/kg [n=7], 0.090 mg/kg [n=9], and 0.110 mg/kg [n=8]). TIMI flow grade 2 or 3 was seen in 1/7 patients receiving zalunfiban at 0.075 mg/kg, in 6/9 patients receiving 0.090 mg/kg, and in 7/8 patients receiving 0.110 mg/kg (ptrend = 0.004). A similar trend was observed based on TIMI flow grade 3. Myocardial perfusion was also related to zalunfiban dose (ptrend = 0.005) as reflected by more frequent TIMI myocardial perfusion grade 3. Consistent with the dose-dependent trends in greater coronary and myocardial perfusion, TIMI thrombus ≥4 grade was inversely related to zalunfiban dose (ptrend = 0.02). CONCLUSION: This post hoc analysis found that higher doses of zalunfiban administered in the cardiac catheterization lab prior to vascular access were associated with greater coronary and myocardial perfusion, and lower thrombus burden at initial angiogram in patients with STEMI undergoing primary percutaneous coronary intervention.

Impact of cardiac history and myocardial scar on increase of myocardial perfusion after revascularization.

PURPOSE: We sought to assess the impact of coronary revascularization on myocardial perfusion and fractional flow reserve (FFR) in patients without a cardiac history, with prior myocardial infarction (MI) or non-MI percutaneous coronary intervention (PCI). Furthermore, we studied the impact of scar tissue. METHODS: Symptomatic patients underwent [15O]H2O positron emission tomography (PET) and FFR before and after revascularization. Patients with prior CAD, defined as prior MI or PCI, underwent scar quantification by magnetic resonance imaging late gadolinium enhancement. RESULTS: Among 137 patients (87% male, age 62.2 ± 9.5 years) 84 (61%) had a prior MI or PCI. The increase in FFR and hyperemic myocardial blood flow (hMBF) was less in patients with prior MI or non-MI PCI compared to those without a cardiac history (FFR: 0.23 ± 0.14 vs. 0.20 ± 0.12 vs. 0.31 ± 0.18, p = 0.02; hMBF: 0.54 ± 0.75 vs. 0.62 ± 0.97 vs. 0.91 ± 0.96 ml/min/g, p = 0.04). Post-revascularization FFR and hMBF were similar across patients without a cardiac history or with prior MI or non-MI PCI. An increase in FFR was strongly associated to hMBF increase in patients without a cardiac history or with prior MI/non-MI PCI (r = 0.60 and r = 0.60, p < 0.01 for both). Similar results were found for coronary flow reserve. In patients with prior MI scar was negatively correlated to hMBF increase and independently predictive of an attenuated CFR increase. CONCLUSIONS: Post revascularization FFR and perfusion were similar among patients without a cardiac history, with prior MI or non-MI PCI. In patients with prior MI scar burden was associated to an attenuated perfusion increase.

Transcatheter edge-to-edge mitral valve repair for post-myocardial infarction papillary muscle rupture and acute heart failure: A systematic review.

Papillary muscle rupture (PMR) is a rare complication of acute myocardial infarction (AMI) associated with high mortality and morbidity. Surgery is the gold-standard treatment for these patients, but it is burdened by a high perioperative risk due to hemodynamic instability. Mitral transcatheter edge-to-edge repair (M-TEER) was reported to be safe and effective in unstable patients with significant mitral regurgitation. However, data in patients with post-AMI PMR are limited to a few case reports. In this review, we summarized all data available regarding percutaneous treatment of post-AMI PMR. These results show that M-TEER is safe and effective in this setting with low in-hospital mortality and complications and high rate of significant mitral regurgitation reduction.

Early Trimetazidine Therapy in Patients Undergoing Primary Percutaneous Coronary Intervention for ST Segment Elevation Myocardial Infarction Reduces Myocardial Infarction Size.

PURPOSE: Trimetazidine, a metabolic agent with anti-ischemic effects, was reported to reduce reperfusion injury in animal models. In this randomized double-blind placebo-controlled trial, we investigated the effects of trimetazidine on the reduction of infarction size in patients undergoing revascularization for ST segment elevation myocardial infarction (STEMI). METHODS: Patients with STEMI randomly received trimetazidine (n = 87) or placebo (n = 86) before primary percutaneous coronary intervention (PCI), and subsequently received oral trimetazidine or placebo for 12 months after reperfusion. The predefined primary endpoint was infarction size on cardiac magnetic resonance (CMR) performed at 7 days after primary PCI. The trial was registered on www. CLINICALTRIALS: gov (registration number: NCT02826616). RESULTS: The clinical characteristics of the patients in both groups were well-matched at baseline. At 7 days after primary PCI, the percentage and absolute infarction size in the trimetazidine group were significantly smaller than those in the control group (22% ± 12% [n = 74] vs. 27% ± 13% [n = 74], p = 0.011 and 28 ± 18 g [n = 74] vs. 35 ± 19 g [n = 74], p = 0.022, respectively), and the incidence of myocardial microvascular obstruction (MVO) measured by CMR was significantly reduced in the trimetazidine group (29.7% [22/74] vs. 52.7% [39/74], p = 0.005). The myocardial salvage index (MSI) measured by CMR was significantly higher in the trimetazidine group (48% ± 20% vs. 39% ± 20%, p = 0.008). The incidence of readmission due to aggravated heart failure did not differ significantly between the trimetazidine group and the control group (8.0% vs. 14.0%, p = 0.234). CONCLUSIONS: In patients with STEMI undergoing primary PCI, early trimetazidine before reperfusion reduced myocardial infarction size and MVO, and improved MSI.

Acute myocardial infarction after a negative Dobutamine stress echocardiogram in a patient with end-stage liver disease.

Dobutamine stress echocardiogram (DSE) is generally a safe and reliable test for detection of myocardial ischaemia. We report the case of a 43-year-old male with end-stage liver disease (ESLD), who underwent DSE as part of workup for liver transplantation. Although the patient had an uneventful negative DSE, within 45 minutes he developed inferior ST-segment elevation myocardial infarction (STEMI). His coronary angiography showed severe 2-vessel coronary artery disease, which was treated with percutaneous coronary intervention (PCI) with implantation of drug-eluting stents (DES). Acute coronary syndrome (ACS) after a normal DSE has previously been reported in the literature. We describe one such case, with added complexity of managing an ACS in a patient with high bleeding risk. Our case is unique in reporting a STEMI after a negative DSE in a liver transplant recipient. Increased physician awareness of potential complications of DSE is essential to allow timely recognition and management.

Increasing myocardial edema is associated with greater microvascular obstruction in ST-segment elevation myocardial infarction.

Microvascular obstruction (MVO) frequently develops after ST-elevation myocardial infarction (STEMI) and is associated with increased mortality and adverse left ventricular remodeling. We hypothesized that increased extravascular compressive forces in the myocardium that arise from the development of myocardial edema because of ischemia-reperfusion injury would contribute to the development of MVO. We measured MVO, infarct size, and left ventricular mass in patients with STEMI (n = 385) using cardiac MRI 2 to 3 days following successful percutaneous coronary intervention and stenting. MVO was found in 57% of patients with STEMI. The average infarct size was 45 ± 29 g. Patients with MVO had significantly greater infarct size and reduced left ventricular (LV) function (P < 0.01) compared with patients without MVO. Patients with MVO had significantly greater LV mass than patients without MVO and there was a linear increase in MVO with increasing LV mass (P < 0.001). Myocardial edema by T2-weighted imaging increased with increasing LV mass and patients with MVO had significantly greater myocardial edema than patients without MVO (P < 0.01). Patients with MVO had significantly greater left ventricular end-diastolic pressure (LVEDP) than patients without MVO (P < 0.05). In a cohort of patients with STEMI who underwent primary percutaneous intervention, we observed that MVO increased linearly with increasing LV mass and was associated with increased myocardial edema and higher LVEDP. These observations support the concept that extravascular compressive forces in the left ventricle may increase with increasing ischemic injury and contribute to the development of MVO.NEW & NOTEWORTHY Patients with STEMI (n = 385) had cardiac MRIs 2 to 3 days following reperfusion with primary PCI to determine the relationship between myocardial edema, LV mass, and MVO. We observed that MVO increased linearly with LV mass and that myocardial edema measured by T2-imaging also increased linearly with LV mass. Patients with MVO had greater edema and LVEDP than subjects without MVO. These findings suggest that myocardial edema which arises from ischemia-reperfusion injury may result in extravascular compression of the microcirculation manifested as MVO on cardiac MRI.

Myocardial infarction with non obstructive coronary arteries complicated with ventricular septal rupture: A case report and literature review.

Ventricular septal rupture represents one of the most serious complications after an acute coronary syndrome. Nowadays this condition is rare due to early revascularization, but is still associated with high mortality rate. In this case report, we present an unusual case of a woman suffering an acute myocardial infarction with normal coronary arteries complicated with a ventricular septal rupture, which required surgical correction.

CoO Nanoparticles Combined with MRI: Analysis of No-Reflow in Patients with Acute ST-Segment Elevation Myocardial Infarction after PCI and the Effect of Coronary Nicorandil.

Magnetic resonance imaging (MRI) has become one of the most important medical imaging techniques in the clinic due to its high degree of soft tissue resolution and no radiation damage, and it plays an important role in the early diagnosis and treatment of tumors. This article mainly studies the analysis of no-reflow in patients with acute ST-segment elevation myocardial infarction after PCI and the effect of coronary nicorandil on CoO nanoparticles combined with MRI. In this paper, the synthesized water-soluble nanoparticles are dispersed in a 2% xanthan gum or agarose solution. In an MRI analyzer, the T1 value is tested with the inversion recovery sequence, and the T2 value is tested with the hard pulse CPMG sequence. The gyroscope imaging sequence performs T1-weighted and T2-weighted imaging tests. Calculated densitometry (QCA) was used to measure the stenosis of the coronary lesions, the length of the lesions and the diameter of the lumen before stent implantation. In order to facilitate the collection of urine samples, this article adopts the method of inserting a catheter to drain the patient for sampling. From the baseline state at the time of enrollment to 150 minutes after PCI, polyethylene containing 0.1% butylated hydroxyanisole is used. Urine samples were taken from the test tube every 30 minutes, a total of 6 times were collected, and the collected urine samples were stored in a low-temperature refrigerator at -80℃ for the final inspection. This paper uses calculation software to calculate the risk of death and death/myocardial infarction in the hospital and at 6 months after discharge. The data showed that the postoperatively detected CKMB and cTnI were higher than those before the operation, but the peak value of the nicorandil group was lower than that of the control group, but there was still no statistical difference (P>0.05). The results show that nicorandil can significantly improve the no-reflow phenomenon in AMI patients during PCI.

Post myocardial infarction left ventricular intramural dissecting hematoma: a case report describing a very rare complication.

BACKGROUND: Dissecting intramural hematoma is a rare complication of acute myocardial infarction (AMI) and has been associated with increased mortality. There has been paucity of literature to establish protocols and guidelines for management in such cases. CASE PRESENTATION: We hereby report the case of a 45-year-old male patient with left ventricular intramural dissecting hematoma (LV-IDH) who presented with chest pain and breathlessness and diagnosed as non-ST-elevation myocardial infarction (NSTEMI). Transthoracic echocardiography (TTE) was performed showing LV-IDH, confirmed with cardiac magnetic resonant imaging (cMRI). Selective coronary arteriography (CAG) was performed showing significant obstructive coronary artery disease (CAD). Further management with conservative approach involved discussion with patient, cardiothoracic surgeon and cardiology team including heart failure specialist and interventional cardiology. CONCLUSIONS: This case describes a rare complication of AMI and also focuses on utility of TTE and cMRI in the diagnosis of this rare complication. Both diagnosis and management are challenging and have to be individualized in similar cases. Multidisciplinary care coordination is important in management of patients with this diagnosis.

Coronary microcirculation dysfunction evaluated by myocardial contrast echocardiography predicts poor prognosis in patients with ST-segment elevation myocardial infarction after percutaneous coronary intervention.

BACKGROUND: The mortality rate of acute ST-segment elevation myocardial infarction (STEMI) remains substantial, despite advances in treatment strategies. Coronary microcirculation dysfunction (CMD) persists after percutaneous coronary intervention (PCI) in a substantial proportion of STEMI patients. The association between CMD assessed using myocardial contrast echocardiography (MCE) and prognosis requires further elucidation. This study aimed to evaluate the impact of CMD after successful PCI on the prognosis of patients with STEMI. METHODS: We enrolled 167 patients with STEMI after PCI who underwent MCE during hospitalization between January 2018 and March 2022. Patients were classified into the CMD and non-CMD groups according to the results of MCE. The clinical data and MCE results of both groups were analyzed. Follow-up was conducted for major adverse cardiac events. RESULTS: MCE detected CMD in 105 patients (62.9%). The CMD group contained fewer hypertensive patients (55.2% versus 74.2%, P = 0.015). Patients with CMD exhibited significantly higher levels of plasma troponin I (TnI) [73.2 (23.0-124.0) versus 28.9 (12.7-80.2) ng/mL, P = 0.004], higher levels of plasma B-type natriuretic peptide [255 (99-641) versus 193 (59-389) pg/mL, P = 0.004], poorer Killip classification (P = 0.038), and different culprit vessels (P < 0.001) compared to the non-CMD group. Patients with CMD exhibited lower left ventricular ejection fraction [50 (43-58) versus 61 (54-67) %, P < 0.001], poorer wall motion score index values (1.68 ± 0.4 versus 1.31 ± 0.26, P < 0.001) and poorer left ventricular global longitudinal strain [-11.2 (-8.7 to -14.1) versus -13.9 (-11.0 to -17.2) %, P < 0.001] compared to the non-CMD group. Patients underwent follow-up for 13 (7-20) months. After adjusting for hypertension, peak TnI level, culprit vessel, and Killip classification, CMD was an independent predictor of total major adverse cardiac events at 13 months' follow-up [adjusted odds ratio (OR), 2.457; 95% confidence interval (CI), 1.042-5.790; P = 0.040], and patients with CMD had a higher risk of hospitalization for heart failure (adjusted OR, 5.184; 95% CI, 1.044-25.747; P = 0.044) and repeat myocardial infarction (adjusted OR, 2.896; 95% CI, 1.109-7.565; P = 0.030). CONCLUSIONS: MCE is a safe and effective method for detecting CMD in patients with STEMI. CMD detected by MCE after successful PCI in patients with STEMI is a common occurrence, which is associated with a significantly worse prognosis, especially hospitalization for heart failure and repeat myocardial infarction.

Echolucent Carotid Plaques Becomes More Echogenic over Time - A 3D Ultrasound Study.

BACKGROUND: Despite the presence of only a few established risk factors, some patients will experience atherosclerotic events. Therefore, methods for improved risk stratification for atherosclerotic events are wanted. We aimed to detect changes in carotid artery atherosclerotic plaque volume and echogenicity over time in patients with an acute thromboembolic event and in patients with chronic atherosclerotic disease, both treated with statin, using a novel 3D ultrasound system. METHODS: We included two cohorts of patients; 70 patients, naïve to statin treatment, admitted with acute, first-time myocardial infarction (aMI), and 69 patients who had been on statin treatment for a minimum of 6 months with chronic peripheral arterial disease (cPAD). 3D ultrasound examination was performed at baseline and after 3 and 12 months. Plaque volume was quantified in 3D ultrasound plaque acquisitions, and echogenicity was assessed using grayscale median (GSM) and normalized with adventitia as reference. RESULTS: The aMI group had darker plaques than the cPAD group at baseline (mean GSM: 60.98, standard deviation (SD): 24.09 vs. 71.75, SD: 21.55; P = 0.006), 3 months (63.64, SD: 20.47 vs. 73.44, SD: 20.46; P = 0.006) and at 12 months follow-up (59.25, SD: 18.07 vs. 71.02, SD: 22.31; P = 0.004). The differences were not significant after adjusting for traditional risk factors. Dividing both groups by the median GSM, the darkest half of the aMI group's had an increase in GSM mainly within the first 3 months (10.49, CI 95%: 2.45 to 18.53; P = 0.012) and hereafter remained unchanged at 12 months follow-up (-0.53, CI 95%: -7.28 to 6.22, P = 0.875). In the darkest cPAD group GSM also increased within 3 months (8.14, CI 95%: 1.85-14.32, P = 0.012) and hereafter stabilized till 12 months (-2.54, CI 95%: -9.62 to 4.53, P = 0.475). Plaque volume did not change in the aMI group from baseline (median: 55.41 mm3, interquartile range (IQR): 24.24-84.31) to 12 months (58.67 mm3, IQR: 31.81-93.51) (P = 0.220) whereas there was a small decrease in the cPAD group from baseline (71.63 mm3, IQR: 40.12-135.61) to 12 months (67.73 mm3, IQR: 31.00-122.38) (P = 0.026). CONCLUSIONS: Echolucent carotid plaque, assessed with the novel 3D matrix ultrasound system, had increasing GSM within 3 months period, indicating stabilization of the more vulnerable plaques in aMI and cPAD patients. Plaque volume decreased over 12 months follow-up in a long-term statin-treated patient with cPAD, but not during the first 12 months statin therapy in patients with aMI.

Large vessel occlusions requiring repeated mechanical thrombectomy caused by silent myocardial infarction in a young adult.

OBJECTIVES: Silent myocardial ischemia, defined as objective evidence of myocardial ischemia without symptoms, is associated with ischemic stroke. Nevertheless, silent myocardial infarction is a rare cause of ischemic stroke, especially in young adults with no medical history. MATERIALS AND METHODS: Herein, we report a young adult patient with acute ischemic stroke treated with repeated mechanical thrombectomy for recurrent large vessel occlusions caused by left ventricular thrombus following a silent myocardial infarction. RESULTS: A 40-year-old man was transferred by ambulance to our hospital because of a generalized seizure. He was diagnosed with cerebral infarction and left middle cerebral artery occlusion. We performed intravenous thrombolysis and mechanical thrombectomy. Recanalization was achieved and his symptoms gradually improved. However, the day after treatment he developed bilateral cerebellar infarction and basilar artery occlusion. We performed a second mechanical thrombectomy and recanalization was achieved. Transthoracic echocardiography revealed a mobile left ventricular thrombus. Although he had no previous chest symptomatic episodes, cardiac examination confirmed myocardial infarction of unknown onset. He was diagnosed with acute ischemic stroke with large vessel occlusions caused by left ventricular thrombus following a silent myocardial infarction. Anticoagulation therapy reduced the amount of thrombus. At 1-year follow-up, he had not experienced any recurrences or symptoms. CONCLUSIONS: Silent myocardial infarction should be considered a cause of ischemic stroke in young adults, even without any vascular risk factors. Recurrent large vessel occlusion may occur in patients with left ventricular thrombus, and repeated mechanical thrombectomy should be considered for treatment.

Catheter ablation of ventricular tachycardia in patients with postinfarction left ventricular aneurysm.

BACKGROUND: While ventricular tachycardia (VT) in the setting of postmyocardial infarction left ventricular aneurysms (LVA) is not uncommonly encountered, there is a scarcity of data regarding the safety, efficacy, and outcomes of ablation of VT in this subset of patients. METHODS: Our study included consecutive patients aged 18 years or older with postmyocardial infarction LVA who presented to Mayo Clinic for catheter ablation of VT between 2002 and 2018. RESULTS: Of 34 patients, the mean age was 70.4 ± 9.1 years; 91% were male. Mean LVEF was 29 ± 9.7% and left ventricular end-diastolic dimension was 64.9 ± 6.6 mm. The site of the LVA was apical in 21 patients (62%). Fifteen patients (44%) presented with electrical storm or incessant VT. Nine patients (26%) had a history of intracardiac thrombus. All except for one patient had at least one VT originating from the aneurysm. The mean number of VTs was 2.9 ± 1.7. All patients underwent ablation at the site of the aneurysm. Ablation outside the aneurysm was performed in 13 patients (38%). Low-voltage fractionated potentials and/or late potentials at the aneurysmal site were present in all cases. Complete elimination of all VTs was achieved in 18 (53%), while the elimination of the clinical VT with continued inducibility of nonclinical VTs was achieved in a further 11 patients (32%). Two patients developed cardiac tamponade requiring pericardiocentesis. During a mean follow-up period of 2.3 ± 2.4 years, 11 patients (32%) experienced VT recurrence. Freedom from all-cause mortality at 1-year follow-up was 94%. CONCLUSION: Radiofrequency catheter ablation targeting the aneurysmal site is a feasible and reasonably effective management strategy for clinical VTs in patients with postinfarction LVA.

Long-term effect of remote ischemic conditioning on infarct size and clinical outcomes in patients with anterior ST-elevation myocardial infarction.

BACKGROUND: Conflicting evidence exists concerning the cardioprotective efficacy of remote ischemic conditioning as an adjunct to primary percutaneous intervention (PCI) in ST-elevation myocardial infarction (STEMI) and data on long-term outcomes are scarce. We evaluated final infarct size by cardiac magnetic resonance (CMR) performed 6 months after anterior STEMI treated with remote ischemic conditioning and clinical outcomes up to 3 years after the event. METHODS: One hundred and fifteen patients with anterior STEMI were randomized to remote ischemic per-postconditioning (RIperpostC) or sham procedure as adjunct to primary PCI. The primary outcome was myocardial salvage index (MSI) on CMR 6 months after the event. Secondary outcomes were absolute infarct size, left ventricular function, cardiac mortality, major adverse cardiac and cerebrovascular events (MACCE-composite of all-cause mortality, myocardial infarction, readmission for heart failure, ischemic stroke, and target lesion revascularization) and all the individual components of MACCE. RESULTS: There was no difference in MSI or left ventricular function between the RIperpostC and the control group after 6 months. Nor did clinical outcomes at 6 months or 3 years differ between the groups. CONCLUSIONS: RIperpostC as an adjunct to PCI in anterior STEMI did not result in better MSI or left ventricular function 6 months after the event. Furthermore, clinical outcomes at 6 months and 3 years were not altered.

Hybrid approach to postmyocardial infarction ventricular septal defect repair.

Postinfarction ventricular septal rupture is a rare and devastating complication of myocardial infarction. Despite attempts at acute surgical and percutaneous defect closure, morbidity and mortality remain high. Herein, we describe a hybrid surgical and catheter-based approach to defect closure in a 63-year-old woman with postinfarction ventricular septal rupture and cardiogenic shock.

Leriche syndrome in a patient with acute pulmonary embolism and acute myocardial infarction: a case report and review of literature.

BACKGROUND: Both acute myocardial infarction and acute pulmonary embolism are distinct medical urgencies while they may conincide. Leriche's syndrome is a relatively rare aortoiliac occlusive disease characterized by claudication, decreased femoral pulses, and impotence. We present the first case of concomitant acute pulmonary embolism, acute myocardial infarction, and Leriche syndrome. CASE PRESENTATION: A 56-year-old male with a history of intermittent claudication was admitted for evaluating the sudden onset of chest pain. Elevated serum troponin level, sustained high D-dimer level, ST-T wave changes on electrocardiogram, and segmental wall motion abnormality of the left ventricle on transthoracic echocardiography were noted. Pulmonary Computed Tomography Angiogram revealed multiple acute emboli. Aortic Computed Tomography Angiogram spotted complete obstructions of the subrenal aorta and bilateral common iliac arteries with collateral circulation, maintaining the vascularization of internal and external iliac arteries. We stated the diagnosis of acute pulmonary embolism and Leriche syndrome and initiated oral anticoagulation. However, Q waves on electrocardiogram and wall motion abnormality on echocardiography persisted after embolus dissolved successfully. Coronary computed tomography angiogram found coronary arterial plaques while myocardial Positron Emission Tomography detected decreased viable myocardium of the left ventricle. We subsequently ratified the diagnosis of concurrent acute pulmonary embolism, acute myocardial infarction, and Leriche syndrome. The patient was discharged and has been followed up at our center. CONCLUSION: We described the first concurrence of acute pulmonary embolism, acute myocardial infarction, and Leriche syndrome.

Giant coronary artery fistula complicated with coronary artery aneurysm and acute myocardial infarction: a case report.

BACKGROUND: Coronary artery fistula (CAF) is an abnormal connection between a coronary artery and either a cardiac chamber or the great vessels. Although most patients are asymptomatic, potential complications such as heart failure, angina pectoris or acute myocardial infarction can be fatal. CASE PRESENTATION: We present here a 62-year-old man diagnosed with giant coronary artery fistula complicated with gross coronary artery aneurysm and acute myocardial infarction. He underwent intravenous thrombolysis treatment at a local hospital, coronary angiography at a regional hospital and complex surgery at a national centre for cardiovascular disease. The patient had no major adverse cardiac events during the 3-year follow-up. CONCLUSION: Early diagnosis of CAF patients and an appropriate treatment plan are the key factors for avoiding serious complications. Because of the rare incidence of this disease, it is necessary to discover and discuss management strategies, including medical management, percutaneous interventions or surgical treatment, for a successful outcome.

Management strategies and clinical outcomes of acute myocardial infarction in leukaemia patients: Nationwide insights from United States hospitalisations.

BACKGROUND: Patients with leukaemia are at increased risk of cardiovascular events. There are limited outcomes data for patients with a history of leukaemia who present with an acute myocardial infarction (AMI). METHODS: We queried the Nationwide Inpatient Sample (2004-2014) for patients with a primary discharge diagnosis of AMI, and a concomitant diagnosis of leukaemia, and further stratified according to the subtype of leukaemia. Multivariable logistic regression was conducted to identify the association between leukaemia and major acute cardiovascular and cerebrovascular events (MACCE; composite of mortality, stroke and cardiac complications) and bleeding. RESULTS: Out of 6 750 878 AMI admissions, a total of 21 694 patients had a leukaemia diagnosis. The leukaemia group experienced higher rates of MACCE (11.8% vs 7.8%), mortality (10.3% vs 5.8%) and bleeding (5.6% vs 5.3%). Following adjustments, leukaemia was independently associated with increased odds of MACCE (OR 1.26 [1.20, 1.31]) and mortality (OR 1.43 [1.37, 1.50]) without an increased risk of bleeding (OR 0.86 [0.81, 0.92]). Acute myeloid leukaemia (AML) was associated with approximately threefold risk of MACCE (OR 2.81 [2.51, 3.13]) and a fourfold risk of mortality (OR 3.75 [3.34, 4.22]). Patients with leukaemia were less likely to undergo coronary angiography (CA) (48.5% vs 64.5%) and percutaneous coronary intervention (PCI) (28.2% vs 42.9%) compared with those without leukaemia. CONCLUSION: Patients with leukaemia, especially those with AML, are associated with poor clinical outcomes after AMI, and are less likely to receive CA and PCI compared with those without leukaemia. A multi-disciplinary approach between cardiologists and haematology oncologists may improve the outcomes of patients with leukaemia after AMI.

Serial assessment of focal myocardial function after percutaneous coronary intervention for ST-elevation myocardial infarction: Value of layer-specific speckle tracking echocardiography.

BACKGROUND: Ischemia-reperfusion injury (IRI) frequently follows successful PCI for STEMI and is recognized by multiple modalities. Multilayer speckle tracking echocardiography (STE) has the potential of detecting myocardial dysfunction in different myocardial layers. Our objective was to describe the changes in layer-specific myocardial function over the 24 hours after successful PCI for ST-elevation myocardial infarction (STEMI). METHODS: Patients (n = 120) with STEMI and no prior myocardial infarction underwent echocardiography prior to PCI, immediately after and at 3- and 24-hours post-PCI. Worsening focal dysfunction (WFD) was defined as an immediate reduction, compared to the pre-PCI value, in the amplitude of endo-myocardial longitudinal strain (endo-MLS) within the infarction territory. RESULTS: Patients with WFD (52%) had further reductions in endo-MLS, mid-MLS, and epi-MLS in the infarction region immediately post-PCI; at 3 hours strain began to improve and continued to improve at 24 hours. Reductions of endo-MLS strain were more evident than those of global, mid-MLS, and epi-MLS. This same pattern was seen in each of the ischemic territories of the anterior descending, circumflex, and right coronary arteries. Immediate improvement in endo-MLS following PCI was seen in 48% of patients. The time from symptom onset to balloon time was markedly longer in those with WFD (P < .0001). CONCLUSIONS: Multilayer SPE is a sensitive method that identifies serial alterations in focal myocardial function following successful PCI for STEMI. Layer-specific reductions in endo-MLS appeared more evident than decreases in global LV strain. Prolonged total ischemic time prior to PCI was directly related to the incidence of WFD.