ST-ELEVATION MYOCARDIAL INFARCTION AND ACUTE ISCHEMIC KIDNEY INJURY

The aim of the study was to investigate specific clinical manifestations, homeostasis indices and parameters of the cardiovascular system in patients with acute ST-elevation myocardial infarction (STEMI) and acute ischemic kidney injury. Methods. 173 patients with STEMI participated in the study. The study group consisted of 111 patients with acute ischemic kidney injury associated with myocardial infarction (MI); 62 patients with MI and normal kidney function were enrolled in the comparison group. Clinical, anthropometric, laboratory, and instrumental diagnostic methods were used. Results. Compared with patients of the MI and normal kidney function group, those with MI and acute ischemic kidney injury had a higher average heart rate, required more prolonged vasopressor and/or inotropic therapy, and more frequently developed tachyarrhythmias with adverse prognostic impact and postinfarction aneurysms. The study revealed that patients of the MI and acute ischemic kidney injury group demonstrated more severe dilatation of the left ventricle (LV), more pronounced reduction in myocardial LV contractility according to echocardiography results; they developed multivessel coronary artery disease more frequently. Furthermore, patients of this group had a higher incidence of infarction-associated artery damage located in the proximal segments of major coronary arteries and more frequently developed thrombotic occlusion in the infarction-affected artery. Patients with MI and acute ischemic kidney injury had higher levels of inflammatory, myocardial necrosis, hemostasis and neurohormonal activation markers. Higher concentration of neutrophil gelatinase-associated lipocalin (uNGAL) was observed in patients with MI and acute ischemic kidney injury; moreover, in 14,1% of patients belonging to this group, elevated levels of this marker preceded the diagnostically significant increase in creatinine concentration and decrease in glomerular filtration rate. Conclusion. In patients with MI, the development of acute ischemic kidney injury was accompanied by more severe clinical manifestations, prognostically adverse indicators of early LV remodeling and coronary arteries disease, enhanced inflammatory processes and neuroendocrine system activity, as well as by elevated levels of myocardial necrosis and blood coagulation activity markers. The present study suggests applying uNGAL as an early marker of acute ischemic kidney injury in patients with MI.

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Persistent Hiccups as the Only Presenting Symptom of ST Elevation Myocardial Infarction

Case Reports in Cardiology ◽

10.1155/2018/7237454 ◽

2018 ◽

Vol 2018 ◽

pp. 1-4

Author(s):

Nasreen Shaikh ◽

Rishi Raj ◽

Srinivas Movva ◽

Charles Mattina

Keyword(s):

Myocardial Infarction ◽

Clinical Manifestations ◽

Foot Ulcer ◽

Kidney Injury ◽

Diabetic Foot Ulcer ◽

Coronary Artery Occlusion ◽

Coronary Intervention ◽

St Elevation Myocardial Infarction ◽

Inferior Wall ◽

St Elevation

Clinical manifestations of acute myocardial infarction can be more than just chest pain. Patients can present with dyspnea, fatigue, heart burn, diaphoresis, syncope, and abdominal pain to name a few. Our patient was a 74-year-old male with a past medical history of type 2 diabetes mellitus, hypertension, hyperlipidemia, and COPD due to chronic tobacco use, who presented with persistent hiccups for 4 days and no other complaints. Coincidently, he was found to have a diabetic foot ulcer with sepsis and acute kidney injury and hence was admitted to the hospital. A routine 12-lead EKG was done, and he was found to have an inferior wall ST elevation myocardial infarction. He underwent diagnostic catheterization which demonstrated 100% right coronary artery occlusion and a thallium viability study which confirmed nonviable myocardium; hence, he did not undergo percutaneous coronary intervention. Elderly patients who present with persistent hiccups should be investigated for an underlying cardiac etiology.

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P6404Myocardial infarction with nonobstructive coronary arteries: does aspirin have a place in the treatment of this entity?

European Heart Journal ◽

10.1093/eurheartj/ehz746.0999 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

J Ferreira ◽

F Freitas ◽

V Goncalves ◽

C Ferreira ◽

J Milner ◽

...

Keyword(s):

Myocardial Infarction ◽

Coronary Arteries ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Kidney Injury ◽

St Elevation Myocardial Infarction ◽

Mortality Data ◽

Long Term Follow Up ◽

St Elevation

Abstract Background Myocardial infarction with nonobstructive coronary arteries (MINOCA) is still a clinical enigma that is being increasingly recognised, as the number of coronary angiographies we perform in our centres also increase. However, the treatment for this entity is still a matter of important debate, not only due to the different causative mechanisms of this disease but also because there are no major trials regarding MINOCA treatment. Purpose To determine the association between acetylsalicylic acid (ASA) use after discharge and mortality after discharge in MINOCA patients admitted to a coronary care unit (CCU). Methods We analyzed data from 370 (11.7% of the global sample) patients admitted with MINOCA in our CCU. Patients with other final diagnoses, missing mortality data, previous acute myocardial infarction, contra-indications to aspirin and known heart failure before admission were excluded. All patients underwent transthoracic echocardiography and coronary angiography at any point during hospitalisation. After adjusting data for relevant comorbidities we then compared mortality after hospital discharge between the ASA group and the no-ASA group. Results Of all MINOCA patients admitted in our CCU, 84 (22.7%) were diagnosed with ST-elevation myocardial infarction (STEMI) and 286 (77.3%) with non-ST elevation myocardial infarction (NSTEMI). 296 (80%) patients received ASA after discharge. Both groups were homogeneous as we did not find any significant differences between groups regarding age (p=0.106), left ventricle ejection fraction (p=0.100), GRACE score at hospitalisation (p=0.150), Killip-Kimball class at hospitalisation (p=0.604), incidence of acute kidney injury (p=0.450), maximum c-reactive protein during stay (p=0.804) and low-density lipoprotein levels at hospitalization (p=0.055). There was also no difference in the incidence of diabetes (p=0.350), exposure to daily stress (p=0.767), active smoking (p=0.569), dyslipidemia (p=0.229), hypertension (p=0.057) and type of myocardial infarction (STEMI vs NSTEMI – p=0.215). In this MINOCA cohort (5 years follow-up) a total of 47 patients died (12.7%). ASA vs. no-ASA 1-month (3.1% vs. 0.0%, p=0.214), 6-month (4.5% vs. 1.4%, p=0.317), 1-year (5.9% vs 5.6%, p=0.900), 3-year (10.5% vs. 8.3%, p=0.668) and 5-year (13.3% vs. 12.5%, p=0.860) all-cause mortality was not significantly different. The same non-significant trend towards higher mortality with ASA was obtained when survival curves were taken into account. Conclusions MINOCA remains a challenging entity. In our study, the systematic use of ASA in all patients following MINOCA was not associated with better survival after long-term follow-up.

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