Recurrent ST Elevation Myocardial Infarction Research Articles

Unchanged cellular inflammatory response following recurrent ST-elevation myocardial infarction

BackgroundRecurrent ST-elevation myocardial infarctions (STEMIs) are associated with poorer prognosis. A diminished haematopoietic response has been proposed as the mechanism responsible for this, but has yet to be validated in human studies. We therefore aim to map out the leukocyte response, and its subtypes, following the first and second STEMI to identify if the inflammatory response is dampened after recurrent myocardial infarctions. MethodsRetrospective cohort study of patients presenting with recurrent STEMI undergoing percutaneous coronary intervention. Full blood counts were taken within 24 h of each admission, and daily thereafter. The primary outcome was whether there were any qualitative or quantitative difference in leukocyte cell response (and its subtypes) between first and second STEMI. ResultsThirty-one patients (mean age 59 years [SD 14.9], 26 males [83.9%]) with an average of 3.1 years between infarcts were included in the study. Overall, between first and second STEMI, similar mean leukocyte response (and its subtypes) was observed from admission to day three post PCI. Similarly, the peak leukocyte response (and its subtypes) was similar between the two STEMIs, even after adjusting for infarct size. ConclusionsIn recurrent STEMIs, there is no long-term memory effect on the cellular inflammatory response leading to diminished peripherally circulating leucocytes, and its subtypes.

Criteria for comparatively evaluating efficacy of treatment for recurrent ST segment elevation myocardial infarction

Hospital mortality rate is considered one of the convincing criteria to assess the efficacy of the treatment for ST-elevation myocardial infarction (STEMI). Among the predictors of the mortality risk (MR), the age over 75 years is the most significant one. The aim of the study was to comparatively assess the treatment efficacy in patients with recurrent STEMI considering the hospital mortality with regard to the baseline MR and/or the age over 75 years in different timeframes in the period from 2008 to 2017. We studied 743 patients with recurrent STEMI admitted at our Institute clinic in the period from 2008 to 2017. The first group consisted of 312 patients hospitalized from 2008 to 2011; 51 of them were over 75 years old. PCI was performed in 71 and 51 cases in the first 12 and 12–72 hours, respectively. The second group included 157 patients who were admitted in the period from 2012 to 2014; 40 of them were over 75 years old, early and delayed PCIs were performed in 57 and 32 patients, respectively. And the third group consisted of 263 patients admitted from 2015 to 2017, among whom 128 patients were over 75 years old; early and delayed PCIs were performed to 82 and 80 patients, respectively. Baseline MR was determined by TIMI. Over 10 years, the number of primary PCIs had increased from 39 % in the first period to 62 % in the third one, and from 3 % to 32 % in patients older than 75 years old. The use of delayed PCI had doubled their total number. Meanwhile, although the angiographic success rate remained unchanged, there was no decrease in hospital mortality. The explanation for this lies in the increased proportion of the hospitalized patients over 75 years of age and higher mortality rates compared to those younger 75 years of age. So, in the older age group, the baseline MR was scored 7.5 or made 25 % by TIMI, the mortality was 18.3 %, making 11.6 % and 25.2 % when the PCI performance and non-performance were taken into account. These figures were 2 times lower among patients younger 75 years of age: initial MR was scored 5 making 12.5 % by TIMI; mortality was 9.6 %, making 6.5 % and 12.5 % for PCI and non-PCI cases, respectively. In this regard, with an increase in the number of hospitalized patients over 75 years of age, a higher number of PCIs performed, which was considered as associated with an increased treatment efficacy, may have not been accompanied by a decrease in hospital mortality. With similar evaluated parameters, the treatment efficacy turns to be higher among the patients with higher MR. The mortality reduction proportional to the baseline MR in different age groups indicates the results of interventions that are similar in their efficacy. These data indicate that the hospital mortality assessment with taking into account the baseline MR and/or age over 75 years, makes it possible to assess the efficacy of treatment for STEMI more objectively, to outline the ways for increasing its efficacy by using PCI in late admission, similar to that in early procedures used without age restrictions.

The Problem of Drug Interactions Between Rosuvastatin and Ticagrelor in the Aspect of the Risk of Rhabdomyolysis: Discussion of the Problem and Description of the Clinical Case

Background. Combination therapy with two antiplatelet agents (ticagrelor or clopidogrel plus acetylsalicylic acid) and a high dose statin is recommended in accordance with clinical guidelines for patients undergoing acute coronary syndrome and coronary intervention. Combined therapeutic regimens have drug-drug interaction potential. Rhabdomyolysis is a known side effect of statin therapy, and there is evidence that co-therapy with ticagrelor increases the risk of this complication.Case description. A 72-year-old female patient was hospitalized with typical signs of rhabdomyolysis: muscle pain, oliguria, weakness, significant increases in creatine kinase (CK), myoglobin and creatinine. One month before that, she was urgently hospitalized with acute recurrent ST-elevation myocardial infarction and underwent endovascular intervention on a critical stenosis of the left anterior descending artery with stent implantation. After that, rosuvastatin 40 mg per day and ticagrelor 90mg 2 times a day were added to her therapy. During the current hospitalization, rosuvastatin, ACE inhibitors and spirolactone were canceled, infusion therapy was carried out, which led to a rapid regression of symptoms, restoration of adequate diuresis, and normalization of CK, myoglobin and creatinine levels. Conclusions. The combined use of ticagrelor with rosuvastatin (especially at a high dose) increases the risk of rhabdomyolysis in elderly patients. Patients taking ticagrelor may require changes in statin therapy, dose adjustments, and possible drug changes to avoid pharmacological interactions and an increased risk of side effects.

Coronary Artery Ectasia Complicated by Recurrent ST-Elevation Myocardial Infarction

Coronary artery ectasia (CAE) is an uncommon cardiovascular disorder characterized by diffuse dilatation of the coronary arteries, which can be complicated by thrombosis and myocardial infarction. We present the case of a 44-year-old man with a history of CAE complicated by prior inferior ST-elevation myocardial infarction, who presented with acute-onset substernal chest pain 3 ​weeks after stopping outpatient apixaban.

Infarct-related artery and long-term mortality following recurrent ST-elevation myocardial infarction; insights from a Polish nationwide registry

Abstract Background Recurrent ST-elevation myocardial infarction (rSTEMI) occurs either as an acute thrombotic event in the same (target-vessel, TV-STEMI) or different vessel (non-target, nonTV-STEMI) compared with the first infarction. Little is known about the frequency of rSTEMI in the era of primary percutaneous coronary intervention (PCI) and about the impact of the infarct-related artery (IRA) on long-term prognosis. Purpose We hypothesized that long-term mortality after rSTEMI varies according to IRA (either same or different compared with first STEMI). Methods We retrospectively analysed data from the Polish Registry of Acute Coronary Syndromes (PL-ACS) and identified survivors of first STEMI treated with PCI who experienced rSTEMI and were discharged home. We divided rSTEMI into TV-STEMI and nonTV-STEMI group. We compared baseline clinical, angiographic and procedural characteristics and utilized propensity score matching to adjust for baseline differences. 1-, 3- and 5-year all-cause mortality was obtained from the Polish National Health Fund. Categorical variables were presented as counts and percentages and compared using Chi2 test. Continuous variables were presented as medians and interquartile ranges and compared using Mann-Whitney test. The registry was approved by local Ethics Committee and meets the conditions of the Declaration of Helsinki Results Between January 2003 and August 2019 a total of 3517 patients (mean age 62.9 years, 75% male) had rSTEMI, of whom 1941 (55%) had TV- and 1576 (45%) had nonTV-STEMI after 615 (77, 1683) days since first infarction (Figure 1). Patients with nonTV-STEMI had higher BMI (27.2 vs 26.8 kg/m2, p=0.03), more hypertension (76.9 vs. 73.5%, p=0.02) and atrial fibrillation (4.7 vs. 3.3%, p=0.04), but had lower left ventricular ejection fraction (43 [35,50] vs. 45 [38,50], p<0.001) compared with TV-STEMI. On coronary angiography nonTV-STEMI had more frequently TIMI flow ≥1 (44.9 vs. 28.0%, p<0.001), multivessel disease (51.8 vs. 41.1%, p=0.003), culprit lesion located in circumflex artery (15.2 vs. 4.8, p<0.001) and more frequently underwent stenting (88.4 vs. 76.1%, p<0.001) compared with TV-STEMI. There was no difference in unadjusted 1-, 3- and 5-year mortality between nonTV-STEMI and TV-STEMI group (14.9 vs. 14.7%, p=0.9; 23.4 vs. 24.2%, p=0.64 and 29.6 vs. 32.9%, p=0.1 respectively). The propensity-score matching of 825 patients with TV- and 826 patients with nonTV STEMI suppressed all baseline differences, but adjusted mortality remained similar between study groups (Figure 1). Conclusion While patients with recurrent nonTV-STEMI have different clinical and angiographic characteristics compared with TV-STEMI, the long-term mortality in these groups is similar. Figure 1 Funding Acknowledgement Type of funding source: None

P6210Pathway of care and life course of patients with recurrent ST-elevation myocardial infarction

Abstract Background We hypothesized that patients having experienced one coronary event in their life must present differences in their pathway of care in the acute phase and within 12-month life course. Purpose This study aimed to compare pathways between current and recurrent Myocardial Infarction. Methods All patients from the OSCAR registry with ST Elevation Myocardial Infarction (STEMI) as final diagnosis from 2013 to 2016 were included. We defined recurrent STEMI as a reinfarction occurring within 12-month post-current-STEMI and STEMI with prior MI occurred before the inclusion date. Results Recurrent STEMI called more often the medical dispatch center (71.32% vs 62.36%, p<0.0001) and benefited from out-of-hospital medical care by Emergency Mobile Services (67.07% vs 59.70%, p=0.0007). The hospital management delays did not differ but the delay symptom-ECG tended to be 26 minutes longer for recurrent STEMI admitted directly to the emergency department (182 [109; 314] vs 156 [89; 291], p=0.0510). They also underwent less percutaneous coronary interventions (PCI) (90,24% vs 95,07%, p<0.0001). At 12 months post-discharge, we observed a better adherence to BASIC-treatment (Beta-blockers, Anti-platelet medications [aspirin, clopidogrel, prasugrel], Statins and Converting Enzyme Inhibitor Combination-treatment) for recurrent STEMI (64,06% vs 52,98%, p=0.0062) but the key lifestyle interventions were less applied. Conclusion Comparison of care and life course of current and recurrent STEMI highlighted a different use of pre-hospital care and hospital resources. They also showed better adherence to BASIC-treatment during recurrent events compared to current STEMI. Acknowledgement/Funding The RESCUe Network is funded by the Regional Agency for Health from Auvergne-Rhône-Alpes region (Agence Régionale de Santé Auvergne-Rhône-Alpes).

Spontaneous coronary collateral recruitment in patients with recurrent ST elevation myocardial infarction (STEMI).

The spontaneous recruitment of acute coronary collaterals in the setting of an ST elevation myocardial infarction (STEMI) is seen frequently in those patients undergoing primary percutaneous coronary intervention (pPCI) and is associated with improved clinical outcomes. However, it is unknown whether in patients who present with a recurrent STEMI, the degree of collateral recruitment remains the same as in the index procedure. We reviewed all patients presenting to our tertiary centre with a STEMI undergoing primary or rescue percutaneous coronary intervention (PCI) from July 2010 until December 2018. We identified patients who presented with a recurrent STEMI following their index procedure. We defined patients with poor collateral recruitment as Rentrop grade 0 or 1, whilst patients with robust collateral recruitment as Rentrop grade 2 or 3. Of the 1795 patients who were identified, there were 27 cases in 25 patients who presented with a repeat STEMI following their index procedure. The median time between cases was 12.8days (IQR 2.3-589.5days). Compared to the index case, there was no statistically significant difference in the degree of collateral recruitment in recurrent presentations (Z = -0.378, p = 0.70). In those patients presenting more than 6months following the index procedure, the median time between cases was 654.5days (IQR 479.5-1151.9). There was no difference in the degree of collateral recruitment in recurrent presentations (Z = 0.000, p = 1.0). Cases which had poorer collateral recruitment in recurrent presentations were less likely to be current smokers (0% vs 50%, p < 0.001) and less likely to have diabetes (0% vs 27.3%, p < 0.05) The recruitment of spontaneous coronary collaterals remains constant in recurrent STEMI presentations suggesting an innate biological process rather than merely a manifestation of alteration of haemodynamic blood flow. Further investigations to identify these processes is required.

Clinical profile and outcomes of patients with recurrent ST elevation myocardial infarction: A prospective observational study

Clinical profile and outcomes of patients with recurrent ST elevation myocardial infarction: A prospective observational study

When the Innocent Bystander Becomes the Culprit: Two Episodes of STElevation Myocardial Infarction with Different Culprit Coronary Arteries in A Single Patient Occurring Two Days a Part

Background: Recurrent ST elevation myocardial infarction (STEMI) with different culprit lesions in a single patient occurring few days apart is uncommon with limited similar cases reported. Case Presentation: This is a case of a 53-year-old male who presented to the Emergency Department with left upper quadrant abdominal pain and an initial electrocardiogram showing ST elevation MI in the anterolateral leads. He underwent successful primary angioplasty of the culprit lesion (LAD) with placement of a single Everolimus drug-eluting stent with plans for staged intervention within a month of the remaining severe lesion in the left circumflex (LCx) artery (non-infarct related vessel). Two days after the initial STEMI, the patient experienced recurrence of abdominal pain with hypotension, and a repeat ECG revealed new ST segment elevation in the inferior leads. A repeat coronary angiogram demonstrated a widely patent stent in the LAD and the previously noted diseased LCx. No other new lesions were noted and the RCA was also patent. The patient then underwent a successful second primary PCI of the previously untreated severe lesion in the LCx. Conclusion: Consecutive episodes of acute myocardial infarction in different coronary arteries occurring within hours to a few days after primary PCI for STEMI is uncommon and can be catastrophic if not detected early. The mechanism and predisposing factors to such event are still unclear. The optimum interventional treatment strategy regarding the immediate management of STEMI in patients with multi-vessel disease remains controversial.

Recurrent ST-elevation Myocardial Infarction in a Patient with Systemic Lupus Erythematosus

Increased atherosclerosis and thrombosis in patients with systemic lupus erythematosus (SLE) commonly cause cardiovascular complications such as myocardial infarction. Mechanism of myocardial infarction is different: Some immunological and genetic causes such as antiphospholipid syndrome, increased inflammation, immune complexes, elevated homocysteine level and Factor V Leiden mutation, play pivotal role in this group of patients. So its treatment shows difference too. Anticoagulant drugs are not recommended for treatment of myocardial infarction in current practice however, main treatment protocol should contain oral anticoagulants such as warfarin after myocardial infarction in this group of patients. Herein, we present a 30 year old SLE patient with recurrent STelevation myocardial infarction due to lack of oral anticoagulant treatment. With the initiation of anticoagulation, the patient has not experienced myocardial infarction again. In this case, we underline the importance of oral anticoagulant therapy after myocardial infarction in patients with SLE.

Recurrent ST Elevation Myocardial Infarction: What is the Aetiology?

Coronary artery disease is a leading cause of morbidity and mortality in the western world. Plaque rupture in an atherosclerotic lesion is the most commonly encountered underlying pathophysiology. Spontaneous coronary dissection can have similar presentation, but we as a community of cardiologists may not be aware of uncommon aetiologies, such as vasculitis presenting as ST elevation myocardial infarction (STEMI). Here we present a case report of a lady, who presented with STEMI on three occasions within five days, due to underlying granulomotosis with polyangiitis (GPA).

243 MONOCYTE SUBPOPULATION COUNTS AND TNF ALPHA ASSOCIATIONS WITH CLINICAL OUTCOME POST ST ELEVATION MYOCARDIAL INFARCTION

Background Monocytes are implicated in the initiation and progression of the atherosclerotic plaque contributing to its instability and rupture. Although peripheral monocytosis has been related to poor clinical outcome post ST elevation myocardial infarction (STEMI), only scarce information is available of mechanisms of this association. Tumour necrosis factor alpha (TNFα) is a key cytokine in the acute phase inflammatory response, and it is predominantly produced by inflammatory macrophages. Little is known about TNFα association with circulating monocyte subpopulations post STEMI. Method A total of 142 STEMI patients (mean age 62±13 years; 72% male) treated with percutaneous revascularization were recruited with blood samples obtained within first 24 hours from the onset and on day 10-14. Peripheral blood monocyte subpopulations were enumerated and characterized using flow cytometry after staining for CD14, CD16 and CCR2 and were defined as: CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR+ (Mon2) and CD14+CD16++CCR2- (Mon3) cells. Plasma levels of TNFα were measured by enzyme-linked immunosorbent assay (ELISA, Peprotec system, UK). Major adverse cardiac events (MACE), defined as recurrent STEMI, new diagnosis of heart failure and death were recorded at follow up, mean of 164±134 days. Results TNFα levels were significantly higher 24 hours post STEMI, compared to day 14 (paired t-test, p <0.001) with day 1 levels weakly correlated with total monocyte count as well as Mon1 (Spearman’s correlation, r=0.19, p=0.02 and r=0.22, p=0.01, respectively). There was no correlation between TNFα and Mon2 or Mon3 subpopulations. TNFα levels were significantly higher in patients with a recorded MACE (n=28, Mann-Whitney test, p<0.001) (figure 1).⇓

Paclitaxel-Eluting Versus Bare-Metal Stents in Acute ST Elevation Myocardial Infarction (STEMI)

Data comparing efficacy and safety of drug eluting stents (DES), particularly paclitaxel stent with bare metal stents (BMS) in the setting of acute ST elevation myocardial infarction (STEMI) is limited and inconclusive. The aim of our study is to compare the efficacy and safety of paclitaxel stent with bare metal stent in acute STEMI. A retrospective cohort study was performed on patients from our single community hospital who participated in the C-PORT trial from January 2003 to May 2005. One hundred forty-three patients treated exclusively with either BMS or paclitaxel DES were included (79 with paclitaxel DES and 64 with BMS) and were followed at 1, 3, and 6 months. The primary outcome was occurrence of major adverse cardiac events defined as cardiac death, STEMI or NSTEMI or the need for target vessel revascularization. Variables were compared using appropriate statistics and event free survival curves were estimated. Baseline clinical characteristics in BMS and paclitaxel DES groups were well matched. No statistical difference between BMS and DES groups in the rate of cardiac death (6% vs. 9%, P = 0.56), STEMI or NSEMI (1.6% vs. 1.3% respectively, P = 0.88) and composite end point (13% vs. 10%, P = 0.65) was observed while a significant reduction in target vessel revascularization was seen in DES group (6% vs. 0% respectively, P = 0.02) was noticed. In our patient group with acute STEMI, the use of paclitaxel DES did not show significant decrease in cumulative end points, cardiac mortality and recurrent STEMI or NSTEMI compared with BMS over a 6-month follow-up period. However, a significant reduction in revascularization of target vessel was seen.

Smoking cessation does not alter ST deviation pattern of recurrent myocardial infarctions

Background Myocardial infarction (MI) may be classified as ST elevation MI (STEMI) or non ST elevation MI (NSTEMI). We used the term recurrent MI (RMI's) to denote repeated MI episodes, in a particular patient, in which a different coronary site is responsible for each episode. Recently we reported that most patients with recurrent MI episodes will have either STEMI's or NSTEMI's but not both. A history of smoking was associated with recurrent STEMI's. Objective To determine whether smoking cessation will alter the type of RMI in patients with an index MI of STE type. Methods The analysis included 128 patients who underwent at least 2 MI episodes. We attempted to include only MI's of native vessels, without the presence of extra cardiac conditions that intensify myocardial ischemia. All 128 patients were active smokers who presented with an index MI of the STE type. Of these patients 94 had recurrent STEMI and 34 had recurrent NSTEMI (STE/NSTE group). Results We identified all patients who were no longer active smokers at the time of the recurrent MI: there were 31 (33%) such patients in the STEMI group and 13 (38%) in the STE/NSTE group ( p = NS). Conclusion Smoking cessation did not influence the type of recurrent MI in these patients.

ST-Deviation Patterns in Recurrent Myocardial Infarctions

Myocardial infarction (MI) may be classified as ST-elevation MI (STEMI) or non-STEMI (NSTEMI). We used the term "recurrent MI" (RMI) to denote repeat MI episodes in a particular patient in which a different coronary site is responsible for each episode. We investigated whether the type of RMI is more likely to be of the same type as the index MI or whether patients may have the 2 types of MI at random. The analysis included 305 patients who had >or=2 MI episodes. Acute MIs were classified as STEMI or NSTEMI. We attempted to include only MIs of native vessels, without the presence of extracardiac conditions that intensify myocardial ischemia. Most patients (76%) had repeat episodes of the same MI type, i.e., STEMI or NSTEMI. Recurrent STEMI occurred in 44% of patients, recurrent NSTEMI in 32%, and STEMI and NSTEMI in 24%. Thus, most patients with RMI episodes will have STEMIs or NSTEMIs but not the 2 types, suggesting a predilection of some patients to repeat episodes of occlusive thrombi and others to repeat episodes of nonocclusive thrombi.

Frequency of Recurrent ST-Elevation Myocardial Infarction After Fibrinolytic Therapy in a Different Territory as a Manifestation of Multiple Unstable Coronary Arterial Plaques

Multiple unstable plaques have been demonstrated by various imaging techniques in culprit and nonculprit arteries in patients with acute coronary syndromes, but the frequency with which clinical manifestations of multiple unstable plaques occur is unclear. To estimate this frequency in patients who present within 6 hours with ST-elevation myocardial infarction, we studied electrocardiograms and cardiac marker levels of 722 patients with suspected reinfarction in the HERO-2 trial of 17,073 patients; this trial compared intravenous bivalirudin with unfractionated heparin before administration of streptokinase. Twenty-six patients (3.6%) developed recurrent ST elevation in a different territory. Of all the patients who developed ST elevation in a different territory, 50% (13 of 26) did so during the 48 hours of randomized antithrombin therapy compared with 29% (140 of 487) of those who developed recurrent ST elevation in the index territory (p = 0.046). Recurrent index territory ST elevation occurred in 392 of 552 patients (71%) with confirmed reinfarction, and ST elevation in a new territory occurred in 21 patients (3.8%) with confirmed reinfarction (2.3% and 0.12% of all HERO-2 enrollees, respectively). These data suggest that clinical manifestation of multiple unstable plaques of recurrent ST elevation and reinfarction in a territory different from that of the index ST elevation myocardial infarction after intravenous fibrinolytic and antithrombin therapies is rare.

Combined aspirin and Clopidogrel resistance associated with recurrent coronary stent thrombosis

We report about a 72-year-old woman who was admitted to our hospital because of an acute ST-elevation myocardial infarction (STEMI). At admission, she received a loading dose of 300 mg Clopidogrel and 500 mg aspirin (ASA) prior to angioplasty with stenting of a 90% diameter stenosis of the proximal right coronary artery. After intervention, 75 mg Clopidogrel and 300 mg ASA OD were continued. Three days later, she developed a recurrent acute STEMI due to stent thrombosis and a second stent implantation was performed. The dose of Clopidogrel and ASA remained unchanged. Three days later, the patient suffered a third STEMI due to a restent thrombosis and additional stent implantation was performed. The dose of Clopidogrel and ASA was increased to 75 mg BD and 500 mg OD. Platelet function analysis and aggregation studies demonstrated dose-independent ASA resistance. ADP-induced aggregation showed a short-term platelet inhibition with subsequent rapid normalisation, thus suggesting Clopidogrel resistance. Therefore, the treatment was changed to coumadin and ASA 100 mg OD. Since then, the patient has been clinically stabile. Our case indicates for the first time the existence of a subgroup of patients with combined Clopidogrel and ASA resistance. We conclude that identification of these patients is required and alternative therapeutic options have to be considered.