Extension Of Myocardial Infarction Research Articles

Spontaneous coronary artery dissection: the role of Coronary CT angiography in the follow-up management

Abstract Funding Acknowledgements Type of funding sources: None. Background Spontaneous coronary artery dissection (SCAD) is one of the causes of acute coronary syndrome (ACS), myocardial infarction (MI) and sudden death (SD). Diagnosis is done with coronary angiography (CA); nevertheless, coronary computed tomography angiography (CCTA) is a new useful tool in the acute diagnosis and at follow-up. Treatment could involve a conservative approach or an invasive approach with percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). Purpose 1) analyze the clinical and CCTA features at baseline of patients with a SCAD diagnosis; 2) evaluate the clinical and anatomic outcome at follow-up of patients with a SCAD diagnosis treated with a conservative or invasive approach; 3) evaluate in the conservative approach treated patients the clinical and anatomic outcome of those dismissed with single or double antiplatelet therapy. Methods A retrospective analysis of 57 patients affected by SCAD followed up with Coronary CT angiography (CCTA) between 2010 and 2022. Clinical and anatomic data were collected at baseline and at the follow-up (FU). The clinical endpoints evaluated were: all cause mortality, hospitalization for cardiovascular cause, SCAD or PCI ex-novo and MI; the anatomic endpoints were: patency of coronary artery and/or stents and length dissection changing from baseline. Results 57 patients were divided in 2 groups: 46 (80,7%) patients underwent a conservative treatment and 11 (19,3%) patients a PCI treatment. Patients treated with PCI has a significative incidence of smokers (45,5% vs 15,2%; p = 0,042), peripherical arteriopathy (18,2% vs 0%; p = 0,034), higher troponin peak (40425,8 vs 13436; p = 0,011) and lower ejection fraction (51,4±11,0 vs 57,1±7,6; p = 0,050). Moreover the PCI population has a significant involvement of more than one coronary artery (72,7% vs 6,5%; p<0,001), of the proximal tracts of the coronary arteries (22,8% vs 13 %; p = 0,001) and of the truncus communis (45,4% vs 0%; p<0,001). At the follow up, there were no statistical differences for the clinical and anatomic endpoints between the conservative and invasive treated patients (p>0,05). Among patients treated with conservative therapy, there were a significant recurrence of SCAD in those treated with DAPT than in those treated with SAPT (33,3% vs 5,9%; p = 0,033). Conclusions patients with SCAD managed with PCI have more cardiovascular risk factors, a major myocardial infarction extension and a more complex coronary arteries involvement; conservative management is comparable to the PCI treatment for the clinical and anatomic endpoints evaluated; DAPT at discharge was associated with a higher rate of SCAD recurrence at follow-up.

C78 SPONTANEOUS CORONARY ARTERY DISSECTION: THE ROLE OF CORONARY CT ANGIOGRAPHY IN THE FOLLOW–UP MANAGEMENT

Abstract Background Spontaneous coronary artery dissection (SCAD) is one of the causes of acute coronary syndrome, myocardial infarction (MI) and sudden death. Although the gold standard for diagnosis is invasive coronary angiography, Coronary Computed Tomography Angiography (CCTA) is a new useful tool for the diagnosis and follow–up (FU). Treatment could involve a conservative or an invasive approach with percutaneous coronary intervention (PCI) or coronary artery bypass grafting. AIMS: 1) analyze the clinical and CCTA features at baseline of patients with SCAD; 2) evaluate the clinical and anatomic patients outcome with conservative or invasive treatment; 3) evaluate in patients treated with the conservative approach the clinical and anatomic features of those dismissed with single (SAPT) or double (DAPT) antiplatelet therapy. Methods Clinical and anatomic data of 57 patients with SCAD, followed up with CCTA enrolled retrospectively between 2010 ad 2022, were collected at baseline and at the FU. The clinical endpoints evaluated were: all causes mortality, hospitalization for cardiovascular cause, SCAD or PCI ex–novo and MI. The anatomic endpoints were: patency of coronary artery and/or stents and length dissection changing from baseline. Results 46 (80,7%) patients underwent a conservative treatment and 11 (19,3%) under PCI. Patients treated with PCI were more smokers (45,5% vs 15,2%; p=0,042), had peripherical arteriopathy (18,2% vs 0%; p=0,034), higher troponin peak (40425,8 vs 13436; p=0,011) and lower ejection fraction (51,4±11,0 vs 57,1±7,6; p=0,050). Moreover the PCI population had a significant involvement of more than one coronary artery (72,7% vs 6,5%; p<0,001), of the proximal tracts of the coronary arteries (22,8% vs 13 %; p=0,001) and of the truncus communis (45,4% vs 0%; p<0,001). At the FU, there were no statistical differences for clinical and anatomic endpoints between the two groups (p>0,05). Among patients treated with conservative therapy, there was a more significant recurrence of SCAD in those treated with DAPT than in those treated with SAPT (33,3% vs 5,9%; p=0,033). Conclusions Patients with SCAD managed with PCI have more cardiovascular risk factors, a major myocardial infarction extension and a more complex coronary arteries involvement; conservative management is comparable to the PCI treatment for the clinical and anatomic endpoints evaluated. DAPT at discharge is associated with a higher rate of SCAD recurrence at FU.

Left Ventricular Adverse Remodeling in Ischemic Heart Disease: Emerging Cardiac Magnetic Resonance Imaging Biomarkers

Post-ischemic left ventricular (LV) remodeling is a biologically complex process involving myocardial structure, LV shape, and function, beginning early after myocardial infarction (MI) and lasting until 1 year. Adverse remodeling is a post-MI maladaptive process that has been associated with long-term poor clinical outcomes. Cardiac Magnetic Resonance (CMR) is the best tool to define adverse remodeling because of its ability to accurately measure LV end-diastolic and end-systolic volumes and their variation over time and to characterize the underlying myocardial changes. Therefore, CMR is the gold standard method to assess in vivo myocardial infarction extension and to detect the presence of microvascular obstruction and intramyocardial hemorrhage, both associated with adverse remodeling. In recent times, new CMR quantitative biomarkers emerged as predictive of post-ischemic adverse remodeling, such as T1 mapping, myocardial strain, and 4D flow. Additionally, CMR T1 mapping imaging may depict infarcted tissue and assess diffuse myocardial fibrosis by using surrogate markers such as extracellular volume fraction, which may predict functional recovery or risk stratification of remodeling. Finally, there is emerging evidence supporting the utility of intracavitary blood flow kinetic energy and hemodynamic features assessed by the 4D flow CMR technique as early predictors of remodeling.

Prognostic value of BNP in STEMI patients

Abstract Funding Acknowledgements Type of funding sources: None. OnBehalf Portuguese Registry of Acute Coronary Syndromes (ProACS) Introduction Brain natriuretic peptide (BNP) is a highly sensitive and specific biomarker on the extension of myocardial infarction, strongly related to short and long-term prognosis in patients with ST elevation myocardial infarction (STEMI). Objective To evaluate diagnostic and prognostic value of BNP levels in a Portuguese cohort of STEMI patients. Material and methods Retrospective analysis of patients admitted with STEMI included in the Portuguese Registry of Acute Coronary Syndromes between 2010-19. Patients were divided in three groups regarding BNP: Group 1 if BNP <100 pg/ml; Group 2 100 ≤ BNP < 400 pg/ml and Group 3 ≥400 pg/ml. Independent predictors of a composite of all-cause mortality and rehospitalization for cardiovascular causes were assessed by multivariate logistic regression. Results 1650 patients were included, mean age 64 ± 13 years, 75.4% male. 39.0% (n = 643) integrated group 1, 39.5% (n = 652) group 2 and 21.5% (n = 355) group 3. Group 3 patients were significantly older (58 ± 11 vs 66 ± 13 vs 72 ± 12 years, p < 0.001), had more classic cardiovascular risk factors, except for smoker status, and more previous history of cardiovascular disease, chronic kidney disease, chronic obstructive pulmonary disease and cancer. Anterior STEMI was the most frequent location (51.1%), however group 3 patients presented with lower systolic blood pressure (136 ± 30 vs 140 ± 31 vs 131 ± 28 mmHg, p < 0.001) and higher heart rate (76 ± 17 vs 77 ± 19 vs 84 ± 26 bpm, p < 0.001) and KK class (KK class > I 5.6 vs 9.5 vs 28.5%, p < 0.001). They also presented higher levels of creatinine (1 ± 0.5 vs 1.2 ± 0.9 vs 1.5 ± 1 mg/dl, p < 0.001) and the lowest levels of hemoglobin (13.5 ± 1.6 vs 12.6 ± 1.9 vs 11.7 ± 2.1 g/dl, p < 0.001). Mean ejection fraction (EF) was lower in group 3 (58 ± 11 vs 53 ± 12 vs 44 ± 13%, p < 0.001). Multivessel disease was more common in group 3 (34.8 vs 44.8 vs 51.3%, p < 0.001), where a higher percentage was proposed to medical therapy (2.8 vs 3.5 vs 8.5%, p < 0.001). In the patients proposed to revascularization, although not statistically significant, there was a trend towards surgical revascularization or hybrid approach. In-hospital complications were more frequent in group 3, especially heart failure (HF) (18.9% mean vs 45.4%, p < 0.001), and mortality was seven times superior in group 3 versus group 1 (1.2% vs. 8.5%, p < 0.001). The composite endpoint of 1-year mortality and cardiovascular rehospitalization occurred in 12%. After propensity score application, the 1-year endpoint total mortality rate and cardiovascular readmission was 20.3%, and higher BNP was associated with higher rates (p < 0.001). Predictor factors for the composite endpoint, evaluated through Cox multivariate regression were previous HF, multivessel disease, EF < 30% and the use of nitrates and aldosterone antagonists. The use of aspirin was a protector factor. Conclusion BNP levels during index hospitalization were a powerful prognostic biomarker for all-cause mortality MACE in patients admitted with STEMI.

The role of end-diastolic myocardial fibre stretch on infarct extension.

Myocardial infarct extension, a process involving the enlargement of infarct and border zone, leads to progressive degeneration of left ventricular (LV) function and eventually gives rise to heart failure. Despite carrying a high risk, the causation of infarct extension is still a subject of much speculation. In this study, patient-specific LV models were developed to investigate the correlation between infarct extension and impaired regional mechanics. Subsequently, sensitivity analysis was performed to examine the causal factors responsible for the impaired regional mechanics observed in regions surrounding the infarct and border zone. From our simulations, fibre strain, fibre stress and fibre stress-strain loop (FSSL) were the key biomechanical variables affected in these regions. Among these variables, only FSSL was correlated with infarct extension, as reflected in its work density dissipation (WDD) index value, with high WDD indices recorded at regions with infarct extension. Impaired FSSL is caused by inadequate contraction force generation during the isovolumic contraction and ejection phases. Our further analysis revealed that the inadequacy in contraction force generation is not necessarily due to impaired myocardial intrinsic contractility, but at least in part, due to inadequate muscle fibre stretch at end-diastole, which depresses the ability of myocardium to generate adequate contraction force in the subsequent systole (according to the Frank-Starling law). Moreover, an excessively stiff infarct may cause its neighbouring myocardium to be understretched at end-diastole, subsequently depressing the systolic contractile force of the neighbouring myocardium, which was found to be correlated with infarct extension.

P4630Prognostic impact of previous Beta-blocker use in STEMI patients

Abstract Introduction Current guidelines support the use of beta-blockers (βB) in patients with Coronary Artery Disease, especially after a Myocardial Infarction (MI). This use is sustained by their ability to block adrenergic hyperstimulation, reducing the potential for arrythmias, myocardial oxygen consumption and infarct extension. However, questions have been raised regarding the impact βB therapy in patients admitted for ST elevation Myocardial Infarction (STEMI). Methods The authors present a retrospective, descriptive and correlational study including all patients admitted for STEMI in a country's Cardiology Departments between the 1st of October 2010 and the 8th of January 2019. A 1-year (1y) follow-up was made through registry consultation and phone call by a Cardiologist. Baseline demographic and clinical characteristics of patients previously medicated with βB (pre- βB) were compared to patients not medicated with βB. The authors performed a univariate and multivariate statistical analysis of in-hospital mortality, as well as 1y mortality and re-admission rate, using SPSS 24,0. Results A total of 7818 patients were included, 1931 (24,7%) of which 1931 (24,7%) were female, with a mean age of 64±14 years. In the studied sample, 1109 patients (14,2%) were previously medicated with βB, which was more common in women (18,1 vs. 12,8%) and patients over 65-years old (16,9% vs. 11,4%). βB were also more prescribed in patients with hypertension, diabetes, dyslipidaemia, previous MI, previous stroke or peripheral atherosclerosis, and renal failure. This group of patients was more frequently medicated with anti-platelets, anti-hypertensives, statins and diuretics (p<0,001). Additionally, they presented more frequently with Left Bundle Branch Block, Atrial fibrillation, Killip-Kimball class >1 and BNP >400 (p<0,001), and had significantly higher rates of ventricular systolic disfunction (p=0,003). These patients were also more commonly diagnosed with multivessel disease (p<0,001), but no differences could be identified regarding success of revascularization. During hospital stay, no significant divergences were found regarding incidence of shock, mechanical complications and AV block, but a higher rate of haemorrhage and transfusion was objectified (p<0,001). Regarding outcomes, on univariate analysis, pre-βB was a strong predictor of higher 1-year mortality (p=0,049) and 1-year readmission (both global and cardiovascular, with p=0,049 and p=0,033, respectively). On multivariate statistical analysis however, pre-βB showed to be a strong independent predictor of lower in-hospital mortality (p=0,023) with differences between groups who suspended and ditn't suspend βB at admission, but had no significant impact on 1-year outcomes. Conclusion In the present study, previous βB therapy showed to have an independent positive impact on in-hospital mortality, but not on 1-year outcomes.

The relationship of macrophage migration inhibitory factor with clinical and anamnestic parameters in patients with ST-segment elevation myocardial infarction

Objective — to investigate the association between levels of the macrophage migration inhibitory factor (MIF) and the clinical and anamnestic parameters in patients with ST segment elevation myocardial infarction (STEMI) and to determine the factors, affecting this relationship.Materials and methods. The study involved 73 patients with previous confirmed STEMI and successful recovery of blood flow (TIMI-III). The mean patients’ age was (58.37 ± 10.34) years. Clinical, anamnestic and biochemical indicators were determined. The level of MIF was studied using the enzyme linked immunoassay method (RayBio® Human MIF ELISA KIT, USA). The general group of patients was divided by the median MIF level: the first group consisted of patients with low or moderate MIF (≤ 2582.80 ng/ml), n = 36, the second group consisted pf patients with high levels of this cytokine (> 2582.80 ng/ml), n = 37. Mono- and multivariate regression analysis was carried out to identify factors, that mostly significantly affected the MIF levels.Results and discussion. The comparison of median values of the MIF levels in STEMI patients revealed the significant increase in MIF levels vs the control group (2582.80 [1308.40—4122.20] and (573.75 [397.80—1016.75] ng/ml, p < 0.001), that confirmed activation of the MIF formation because of the index event. Positive correlation was determined between the MIF levels, levels of troponin I (r = 0.33; p = 0.045) and blood leukocytes (r = 0.36; p = 0.039). Anterior myocardial infarction (p = 0.047) and injury of left anterior descending artery (p = 0.016) were detected more frequently in the group of patients with high MIF levels, that indicates its directly connection with the size of the myocardial infarction in combination with significantly higher troponin level. Multivariate and univariate logistic analysis showed the reliable independent association between the anterior localization of the MI and the elevated MIF level (OR = 0.2282, 95 % CI [0.1035—0.7680], p = 0.0133), as well as the presence of stable angina to the index event and the lower level of cytokine (OR = 0.2318, 95 % CI [0.0637—0.8438], p = 0.0266).Conclusions. The macrophage migration inhibitory factor at STEMI is involved in the processes of inflammation and necrosis, its increase indicates the direct relationship with the myocardial infarction extension. The presence of stable angina prior the myocardial infarction promotes the pre-conditioning effect and a lower degree of damage, and proportionally lower MIF levels.

TCT-135 The index of microvascular resistance as a surrogate for myocardial infarct extension and microvascular obstruction in patients with ST elevation myocardial infarction treated by primary angioplasty

The index of microcirculatory resistance (IMR) is an invasive surrogate of coronary microvascular function and and an early marker of cardiac recovery, after acute ST elevation myocardial infarction (STEMI), as evaluated by echocardiography. Our purpose in the current study was to confirm its

Early peripheral endothelial dysfunction predicts myocardial infarct extension and microvascular obstruction in patients with ST-elevation myocardial infarction

Introduction and ObjectivesThe role of endothelial dysfunction (ED) in patients with ST-elevation myocardial infarction (STEMI) is poorly understood. Peripheral arterial tonometry (PAT) allows non-invasive evaluation of ED, but has never been used for this purpose early after primary percutaneous coronary intervention (P-PCI). Our purpose was to analyze the relation between ED assessed by PAT and both the presence of microvascular obstruction (MVO) and infarct extension in STEMI patients. MethodsED was assessed by the reactive hyperemia index (RHI), measured by PAT and defined as RHI <1.67. Infarct extension was assessed by troponin I (TnI) release and contrast-enhanced cardiac magnetic resonance (ceCMR). MVO was assessed by ceCMR and by indirect angiographic and ECG indicators. An echocardiogram was also performed in the first 12 h. ResultsWe included 38 patients (mean age 60.0±13.7 years, 29 male). Mean RHI was 1.87±0.60 and 16 patients (42.1%) had ED. Peak TnI (median 118 mg/dl, IQR 186 vs. 67/81, p=0.024) and AUC of TnI (median 2305, IQR 2486 vs. 1076/1042, p=0.012) were significantly higher in patients with ED, who also showed a trend for more transmural infarcts (63.6% vs. 22.2%, p=0.06) and larger infarct mass on ceCMR (median 17.5%, IQR 15.4 vs. 10.1/10.3, p=0.08). Left ventricular ejection fraction (LVEF) was lower and wall motion score index (WMSI) was higher on both echocardiogram and ceCMR in patients with ED. On ceCMR, MVO was more frequent in patients with RHI <1.67 (54.5% vs. 11.1%, p=0.03). ECG and angiographic indicators of MVO all showed a trend toward worse results in these patients. ConclusionsThe presence of ED assessed by PAT 24 h after P-PCI in patients with STEMI is associated with larger infarcts, lower LVEF, higher WMSI and higher prevalence of MVO.

Early peripheral endothelial dysfunction predicts myocardial infarct extension and microvascular obstruction in patients with ST-elevation myocardial infarction

Introduction and ObjectivesThe role of endothelial dysfunction (ED) in patients with ST-elevation myocardial infarction (STEMI) is poorly understood. Peripheral arterial tonometry (PAT) allows non-invasive evaluation of ED, but has never been used for this purpose early after primary percutaneous coronary intervention (P-PCI). Our purpose was to analyze the relation between ED assessed by PAT and both the presence of microvascular obstruction (MVO) and infarct extension in STEMI patients. MethodsED was assessed by the reactive hyperemia index (RHI), measured by PAT and defined as RHI <1.67. Infarct extension was assessed by troponin I (TnI) release and contrast-enhanced cardiac magnetic resonance (ceCMR). MVO was assessed by ceCMR and by indirect angiographic and ECG indicators. An echocardiogram was also performed in the first 12 h. ResultsWe included 38 patients (mean age 60.0±13.7 years, 29 male). Mean RHI was 1.87±0.60 and 16 patients (42.1%) had ED. Peak TnI (median 118 mg/dl, IQR 186 vs. 67/81, p=0.024) and AUC of TnI (median 2305, IQR 2486 vs. 1076/1042, p=0.012) were significantly higher in patients with ED, who also showed a trend for more transmural infarcts (63.6% vs. 22.2%, p=0.06) and larger infarct mass on ceCMR (median 17.5%, IQR 15.4 vs. 10.1/10.3, p=0.08). Left ventricular ejection fraction (LVEF) was lower and wall motion score index (WMSI) was higher on both echocardiogram and ceCMR in patients with ED. On ceCMR, MVO was more frequent in patients with RHI <1.67 (54.5% vs. 11.1%, p=0.03). ECG and angiographic indicators of MVO all showed a trend toward worse results in these patients. ConclusionsThe presence of ED assessed by PAT 24 h after P-PCI in patients with STEMI is associated with larger infarcts, lower LVEF, higher WMSI and higher prevalence of MVO.

Heart rate as a therapeutic target after acute coronary syndrome and in chronic coronary heart disease

For patients with stable coronary artery disease (SCAD), either after hospitalization for acute cardiac events or in the chronic phase, comprehensive treatment programs should be devoted to: (i) reducing mortality and major adverse cardiovascular events, (ii) reducing the ischemic burden and related symptoms, and (iii) increasing exercise capacity and quality of life.Heart rate (HR) has demonstrated to have prognostic value and patients beyond the limit of 70 bpm display increased risk of all the above adverse outcomes, even after adjustment for parameters such as the extension of myocardial infarction and the presence of heart failure. It is well known that a sustained HR elevation may contribute to the pathogenesis of SCAD, being the likelihood of developing ischemia, plaque instability, trigger for arrhythmias, increased vascular oxidative stress, and endothelial dysfunction the mechanisms resulting in this effect. Moreover, high HR could promote chronotropic incompetence, leading to functional disability and reduced quality of life.Despite the strong relationship between HR and prognosis, there is heterogeneity among current guidelines in considering HR as a formal therapeutic target for secondary prevention in SCAD, as far as the cut-off limit. This expert opinion document considered major trials and observational registries in the modern treatment era with beta-blockers and ivabradine, suggesting that an adequate HR control could represent a target for (i), (ii), and (iii) therapeutic goals in SCAD patients with systolic dysfunction (with major evidence for reduced left ventricular ejection fraction <40%), and a target for (ii) and (iii) goals in SCAD patients with preserved left ventricular ejection fraction. The defined cut-off limit is 70 bpm. To date, there is room for improvement of HR control, since in contemporary SCAD patients HR values <70 bpm are present in less than half of cases, even in the vulnerable phase after an acute coronary syndrome.

Endothelial dysfunction evaluated by peripheral arterial tonometry is related with peak TnI values in patients with ST elevation myocardial infarction treated with primary angioplasty

PurposeThe role of endothelial-dependent function in patients with acute ST elevation myocardial infarction (STEMI) is not clear. Endothelial dysfunction may contribute to the pathophysiological processes occurring after STEMI and influence the extension of myocardial necrosis. Endothelial-dependent dysfunction evaluated by peripheral arterial tonometry (PAT) has already showed to be correlated with microvascular coronary endothelial dysfunction. Our purpose was to evaluate the impact of endothelial dysfunction on peak Troponin I (TnI) values, as a surrogate for the extension of myocardial infarction, in patients with STEMI treated with primary angioplasty (P-PCI). Methods58 patients with STEMI treated with P-PCI (mean age 59.0±14.0years, 46 males) were included. Endothelial function was assessed by reactive hyperaemia index (RHI) determined by PAT. Patients were divided in two groups according to the previously reported RHI threshold for high risk (1.67). The extension of myocardial necrosis was evaluated by peak TnI levels. ResultsRHI median value was 1.78 (IQR 0.74); 25 patients had endothelial dysfunction (RHI<1.67). The two groups had no significant differences in age, gender, main risk factors and pain-to-balloon time. Patients with an RHI<1.67 had significant larger infarcts: TnI 73.5ng/mL (IQR 114.42ng/mL) versus TnI 33.2ng/mL (IQR 65.2ng/mL); p=0.028. On multivariate analysis, the presence of an RHI<1.67 kept significant impact on TnI peak values (p=0.02). ConclusionsThe presence of endothelial-dependent dysfunction, assessed by PAT, is related with higher peak TnI values in STEMI patients treated with P-PCI. These results strength the possibility that endothelial-dependent dysfunction may be a marker of poor prognosis and eventually a therapeutic target in patients with STEMI.

TCT-604 Impact of endothelial dysfunction evaluated by peripheral arterial tonometry in the extension of ST elevation myocardial infarction treated with primary angioplasty

The role of endothelial function in patients with acute ST elevation myocardial infarction (STEMI) is not clear. The presence of endothelial dysfunction may eventually contribute the pathophysiological processes occurring after STEMI and, consequently, influence the extension of myocardial necrosis

Exercise training prior to myocardial infarction attenuates cardiac deterioration and cardiomyocyte dysfunction in rats

OBJECTIVES:The present study was performed to investigate 1) whether aerobic exercise training prior to myocardial infarction would prevent cardiac dysfunction and structural deterioration and 2) whether the potential cardiac benefits of aerobic exercise training would be associated with preserved morphological and contractile properties of cardiomyocytes in post-infarct remodeled myocardium.METHODS:Male Wistar rats underwent an aerobic exercise training protocol for eight weeks. The rats were then assigned to sham surgery (SHAM), sedentary lifestyle and myocardial infarction or exercise training and myocardial infarction groups and were evaluated 15 days after the surgery. Left ventricular tissue was analyzed histologically, and the contractile function of isolated myocytes was measured. Student's t-test was used to analyze infarct size and ventricular wall thickness, and the other parameters were analyzed by the Kruskal-Wallis test followed by Dunn's test or a one-way analysis of variance followed by Tukey's test (p<0.05).RESULTS:Myocardial infarctions in exercise-trained animals resulted in a smaller myocardial infarction extension, a thicker infarcted wall and less collagen accumulation as compared to myocardial infarctions in sedentary animals. Myocardial infarction-induced left ventricular dilation and cardiac dysfunction, as evaluated by +dP/dt and -dP/dt, were both prevented by previous aerobic exercise training. Moreover, aerobic exercise training preserved cardiac myocyte shortening, improved the maximum shortening and relengthening velocities in infarcted hearts and enhanced responsiveness to calcium.CONCLUSION:Previous aerobic exercise training attenuated the cardiac dysfunction and structural deterioration promoted by myocardial infarction, and such benefits were associated with preserved cardiomyocyte morphological and contractile properties.

The Opioid Effects On The Cardiac Markers And Left Ventricular Contractility In Acute Myocardial Infarction Patients

Background: Coronary artery disease is one of the most expensive diseases in the world and one of the most common causes of mortality in Iran and Lorestan state. The association between this disease and its risk factors like smoking was established. According to non medical consumption of opium in many parts of our state, we decided to perform a research in order to evaluate the opioid effects on myocardial infarction (MI) extension. Material & methods: In this descriptive analytical study, we assessed 60 patients with MI admitted in the CCU ward of Imam Khomeini Hospital. The diagnosis of MI was based on their medical history, ECG changes and cardiac enzymes approved by the same cardiologist. Then the consumption of opioid by the patients was evaluated by a questionnaire. According to opioid consumption the patients were divided into two groups. The peak amount of the CPK, CKmb and LDH enzymes and ejection fraction were recorded into two groups during their hospitalizations. Results: The mean peak of CPK and CKmb in the user opium group and in the nonuser were 1075, 152 and 906, 102 respectively. The mean peak of LDH in the users and nonusers were reported 1400 and 1029 respectively. There are significant differences between the measured enzymes between the two groups (P=0.001). Conclusions: According to the effects of opioid on the cardiac enzymes and probably on the MI extension, opioid consumption could be preventative for MI complications.

Temporal changes and interaction of serum cytokines in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention

To investigate the temporal changes of serum cytokines IL-6, IL-8, MCP-1 and IL-10 immediately before and after primary PCI (percutaneous coronary intervention) in patients with ST-segment elevation myocardial infarction (STEMI) and explore the interaction of these cytokines. A total of 59 STEMI patients were recruited. And their serum concentrations of IL-6, IL-8, MCP-1 and IL-10 were measured by ELISA before primary PCI and 4-6 hours, 12 hours, 24 hours and 7 days post-intervention. For each cytokine, the level at each time-point post-PCI was compared to that at pre-PCI. Correlation coefficient test was used to analyze the interactions of these four cytokines. At 12 hours post-PCI, the median serum levels of IL-6 and IL-8 were higher than those before PCI (IL-6: 8.51 ng/L vs 6.76 ng/L, IL-8: 4.67 ng/L vs 2.95 ng/L, both P < 0.05). At 4-6 hours and 12 hours post-PCI, the median values of MCP-1 were increasing significantly compared to those at pre-PCI (35.04 ng/L, 34.24 ng/L vs 30.45 ng/L, both P < 0.05) while those of IL-10 decreased (18.15 ng/L, 18.82 ng/L vs 20.95 ng/L, both P < 0.05). The levels of IL-6 and IL-10 at pre-PCI were associated with the Killip classification on admission (IL-6: r = 0.293, P < 0.05; IL-10: r = -0.287, both P < 0.05). Except for IL-8, other cytokines had no significant relation with the time length from onset to admission (P > 0.05). Additionally, these four cytokines were not found to be related with the location and extension of myocardial infarction, ejection fraction and NT-proBNP. At each time-point, there were a positive relationship among the natural logarithms of the concentrations of IL-6, IL-8 and MCP-1 (P < 0.01), all of which were inverse to the natural logarithm of the concentration of IL-10 (P < 0.01). The pro-inflammatory cytokines increase while the anti-inflammatory cytokines decrease after myocardial ischemia/reperfusion. An imbalance of inflammatory cytokines may be present.

Speckle tracking imaging improves in vivo assessment of EPO-induced myocardial salvage early after ischemia-reperfusion in rats

A noninvasive assessment of infarct size and transmural extension of myocardial infarction (TEMI) is fundamental in experimental models of ischemia-reperfusion. Conventional echocardiography parameters are limited in this purpose. This study was designed to examine whether speckle tracking imaging can be used in a rat model of ischemia-reperfusion to accurately detect the reduction of infarct size and TEMI induced by erythropoietin (EPO) as early as 24 h after reperfusion. Rats were randomly assigned to one of three groups: myocardial infarction (MI)-control group, 45 min ischemia followed by 24 h of reperfusion; MI-EPO group, similar surgery with a single bolus of EPO administered at the onset of reperfusion; and sham-operated group. Short-axis two-dimensional echocardiography was performed after reperfusion. Global radial (GS(r)) and circumferential (GS(cir)) strains were compared with infarct size and TEMI assessed after triphenyltetrazolium chloride staining. As a result, ejection fraction, shortening fraction, GS(r), and GS(cir) significantly correlated to infarct size, whereas only GS(r) and GS(cir) significantly correlated to TEMI. EPO significantly decreased infarct size (30.8 + or - 3.5 vs. 56.2 + or - 5.7% in MI-control, P < 0.001) and TEMI (0.37 + or - 0.05 vs. 0.77 + or - 0.05 in MI-control, P < 0.001). None of the conventional echocardiography parameters was significantly different between the MI-EPO and MI-control groups, whereas GS(r) was significantly higher in the MI-EPO group (29.1 + or - 4.7 vs. 16.4 + or - 3.3% in MI-control; P < 0.05). Furthermore, GS(cir) and GS(r) appeared to be the best parameters to identify a TEMI >0.75 24 h after reperfusion. In conclusion, these findings demonstrate the usefulness of speckle tracking imaging in the early evaluation of a cardioprotective strategy in a rat model of ischemia-reperfusion.

Low dose prospective ECG-gated delayed enhanced dual-source computed tomography in reperfused acute myocardial infarction comparison with cardiac magnetic resonance

Purpose To determine whether prospective electrocardiogram (ECG)-gated delayed contrast-enhanced dual-source computed tomography (DCE-DSCT) can accurately delineate the extension of myocardial infarction (MI) compared with delayed enhanced cardiac MR (DE-MR). Material and methods Eleven patients were examined using dual-source CT and cardiac MR in 2 weeks after a first reperfused MI. DCE-DSCT scan protocol was performed with prospective ECG-gating sequential scan model 7 min after contrast administration. In a 17-model, infarcted myocardium detected by DE-MR was categorized as transmural and subendocardial extension. Segment of infarcted location and graded transmurality were compared between DCE-MDCT and DE-MR. Results In all eleven patients, diagnostic quality was obtained for depicting delayed enhanced myocardium. Agreement between DCE-DSCT and MR was good on myocardial segment based comparison (kappa = 0.85, p < 0.001), and on transmural and subendocardial infarction type comparison (kappa = 0.82, p < 0.001, kappa = 0.52, p < 0.001, respectively). CT value was higher on infarcted region than that of normal region (100.02 ± 9.57 HU vs. 72.63 ± 7.32 HU, p < 0.001). Radiation dose of prospectively ECG-gating protocol were 0.99 ± 0.08 mSv (0.82–1.19 mSv). Conclusions Prospective ECG-gated DCE-DSCT can accurately assess the extension and the patterns of myocardial infarction with low radiation dose.

Scintigraphic evaluation of routine filterwire distal protection in percutaneous coronary intervention for acute ST-segment elevation myocardial infarction: a randomized controlled trial

AimDistal embolization during primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) may result in reduced myocardial perfusion, infarct extension and impaired prognosis. In a prospective randomized trial, we assessed the effect of routine filterwire distal protection on scintigraphic estimated infarct size. Methods and resultsThe effect of routine filterwire distal protection was evaluated in 344 patients with STEMI <12 hours undergoing primary PCI. Patients were randomized to distal protection with a filterwire or standard PCI. The primary endpoint was myocardial infarct size measured by Sestamibi SPECT after 30 days (%). Secondary endpoints included myocardial salvage, ST-segment resolution (STR), myocardial biomarker release and major adverse cardiac and cerebral events. Baseline characteristics including area at risk (estimated by Sestamibi SPECT) were similar. Final infarct size was not statistically different in the distal protection and the control groups (median [IQR], 6% [1-19] and 5% [1-14], P = .23). Also, secondary endpoints were similar in the two treatment groups. ConclusionDistal protection with a filterwire performed as routine therapy in primary PCI for STEMI did not reduce myocardial infarct size. The study does not support routine use of distal protection in primary PCI.

NT-proBNP on admission for early risk stratification in STEMI patients submitted to PCI. Relation with extension of STEMI and inflammatory markers

The prognostic implications of NT-proBNP measured on admission in patients with the ST-elevation myocardial infarction (STEMI) are not so far well elucidated. The present investigation, performed in 198 STEMI patients submitted to percutaneous coronary intervention (PCI), was aimed at assessing the prognostic value of NT-proBNP measured on admission to Intensive Cardiac Care Unit (ICCU) and its relation with the extension of myocardial infarction (indicated by cardiac biomarkers and ejection fraction) and inflammatory markers (C-reactive protein — CRP, erythrocyte sedimentation rate — ESR, leucocytes, fibrinogen). All patients who died during ICCU stay had increased values of NT-proBNP. Each quartile of NT-proBNP resulted directly correlated with age, heart rate, peak Tn I, admission creatinine serum levels, ESR, fibrinogen, and inversely correlated with ejection fraction. At backward logistic regression analysis, NT-proBNP values showed a significative correlation with peak Tn I (OR 1.013; 95% CI 1.001–1.025; p=0.036), and CRP positive (OR 6.450; 95% CI 1.714–24.272; p=0.006); age was close to reaching statistical significance (OR 1.043; 95% CI 0.999–1.089; p=0.055). At long term-follow-up NT-proBNP lacks any prognostic role in predicting adverse events such as hospitalization for rePCI, re-infarction and heart failure. Kaplan–Meier curves showed that all patients dead at follow-up were in the highest NT-proBNP quartiles.