This is a retrospective cohort study. Between 1 January and 31 December of 2020, 524 patients with AMI were admitted to the Cardiology Clinic of the Timisoara Institute of Cardiovascular Diseases within the first 12 hours of the onset of the symptoms. In the absence of contraindications, urgent percutaneous coronary intervention (PCI) was done.

The initial evaluation was grounded on the analysis of low and/or high-probability features resulting from symptoms and signs at presentation, 12-lead ECG, and cardiac troponin [4, 5]. The diagnosis of STEMI was grounded on the existence of at minimum 2 of these 3 parameters: (1) typical angina lasting for more than 20 minutes; (2) ST-segment elevation $\ge$1 mV, lasting for $>$0.08 sec after the J point, in minimum 2 contiguous leads; (3) temporary increase in cardiac enzymes to at least twofold the upper normal laboratory range [4]. NSTEMI was defined when ST-segment depression or deep T‑wave inversion were observed on the ECG, without ST-segment elevation, and/or the biomarkers of myocardial necrosis were increased (e.g., troponin I $\ge$1 $\mu$g/L in our laboratory), in an adequate clinical background (chest pain or angina correspondent) [5].

The PCI was performed and the associated pharmacological treatment was administered according to the European Society of Cardiology (ESC) guidelines [4, 5]. All patients were given a loading dose of 300–600 mg clopidogrel. They habitually received before PCI 5000 IU unfractionated heparin and 300–500 mg aspirin. Glycoprotein IIb/IIIa inhibitors were administered when the operator considered it necessary. If a coronary stent was implanted, clopidogrel was prescribed for 12 months, associated with aspirin.

The inclusion criteria were a confirmed diagnosis of AMI in patients hospitalized within the first 12 hours of the symptoms onset and the absence of exclusion criteria.

Exclusion criteria were: PCI‑related or CABG-related AMI, the presence of diseases worsening the long‑term prognosis such as severe primary cardiomyopathy, severe valvular diseases or congenital heart diseases, kidney dysfunction, liver cirrhosis, a malignant tumor, and severe infection.

The study was advised by the Ethics Commission of the Victor Babes” University of Medicine and Pharmacy. All patients provided written informed consent for participation in the study, in accordance with the Human Rights Declaration of Helsinki.

Baseline data were taken from hospital records and comprised gender, age, Killip functional class on admission, medical history, 12 leads resting electrocardiogram, laboratory data, echocardiographic data, and the results of the coronary angiography.

Medical history integrated information about smoking status, obesity, diabetes, old myocardial infarction, history of stroke, hypertension, peripheral artery disease, chronic obstructive pulmonary disease, chronic kidney disease. The cardiac biomarkers determined at admission were: MB fraction of creatine kinase (CK) and cardiac troponin levels. Further laboratory records were: blood cell count, serum hemoglobin, serum glucose, serum creatinine, estimated glomerular filtration, serum electrolytes, and lipogram.

Medical treatment reports were accomplished at discharge and at the 1-year follow-up.

The cause of death was determined from hospital records, or by a phone conversation with the patient‘s physician for those who died at home.

All causes of readmissions were noted during the 1-year follow-up period. The causes of readmissions were determined by utilizing the hospital records.

The primary endpoint was in-hospital mortality, stated as the death of any cause in the course of the hospitalization for AMI. As cardiac deaths were regarded as those due to AMI, heart failure, cardiogenic shock, acute pulmonary edema, cardiac rupture, or ventricular fibrillation. Noncardiac deaths were stated as deaths having an extra-cardiac cause, e.g., stroke, sepsis, acute renal failure.

The secondary endpoints were mortality and readmission rates throughout the 1-year follow-up phase. 1-year mortality included all-cause (cardiac and non-cardiac) deaths. 1-year readmissions included as causes recurrent myocardial infarction (MI), stent thrombosis, stroke, and bleeding. Recurrent MI was defined using the Academic Research Consortium criteria [6]. Bleeding complications were stated using the Bleeding Academic Research Consortium and the Thrombolysis In Myocardial Infarction bleeding classifications [7, 8]. Stroke was diagnosed in the presence of an irreversible neurological deficit, as stated by a neurologist, and based on supporting evidence, such as brain images.

Important coronary stenosis was stated when a reduction in the internal diameter of at least 75% in the anterior descending, circumferential or right coronary artery and at least 50% in the left main coronary trunk was seen. Multivessel coronary artery disease was stated when important stenosis in several coronary arteries was documented [4, 5].

PCI-related AMI (type 4) was defined as an AMI occurring $\le$48 hours after the index procedure, associated with an increase of cardiac troponin values $>$5 times 99th percentile upper range level (URL) [9].

CABG-related AMI (type 5) was defined as an AMI occurring $\le$48 hours after the index procedure associated with an elevation of cardiac troponin levels values $>$10 times 99th percentile U.R.L [9].

A patient was stated to be hypertensive when his blood pressure was $\ge$140/90 mmHg during hospitalization, when previously diagnosed with hypertension, or when taking antihypertensive medication [10]. Valvulopathies were diagnosed by history, physical examination, and echocardiography [11]. The diagnosis of peripheral artery disease diagnosis was grounded on history, physical examination, ankle-brachial index, and Duplex ultrasound [12]. Hypercholesterolemia was stated by history, the current use of lipid‑lowering agents, or laboratory determinations (total cholesterol $\ge$6.22 mmol/L or low‑density lipoprotein cholesterol $\ge$4.14 mmol/L [13]. Chronic kidney disease was diagnosed when the estimated glomerular filtration rate was below 60 mL/min/1.73 m${}^2$ [14]. Obesity was defined when the body mass index exceeded 30 kg/m${}^2$ [15]. Diabetes mellitus was diagnosed when glycated hemoglobin was $\ge$6.5%, fasting plasma glucose level $\ge$7.0 mmol/L (126 mg/dL), or when plasma glucose was $\ge$11 mmol/L (200 mg/dL) at two hours after 75 g oral glucose load [15]. Chronic obstructive pulmonary disease diagnosis was based on GOLD criteria [16].

Echocardiographic examination was performed during the first 24 hours of hospital admission, using a VIVID S5 ultrasonograph device. LVEF was calculated using the Simpson method. The E/A ratio was determined by means of the antegrade mitral flow [17].

We used the classification the Killip classification of heart failure severity in AMI patients [18].

Data were collected and analyzed using the MedCalc Statistical Software version 19.1.7 (MedCalc Software Ltd, Ostend, Belgium) for Windows. Data are given as mean $\pm$ SD for continuous variables, and as frequencies and percentages for categorical variables. The comparisons between two groups of continuous data were analyzed using t‑tests, while the comparisons of categorical data were studied using Chi‑square tests. To evaluate the participation of each parameter in the evaluated outcomes, univariate and multivariate logistic regression models were used. Cox regression analysis was performed to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). All basal parameters that could be associated with hospital readmission at univariate analysis were included in multivariate logistic regression analysis with the forward stepwise method. The discriminative capacity of the analyzed parameters was assessed by means of the receiver operating characteristic (ROC) curves. The threshold for statistical significance was established at a P-value of 0.05. All P-values were results of two-tailed tests.

Of the 522 admitted with ACS, 476 were registered in the research. The mean age was 67.38 $\pm$ 13.4 years (32–95 years). 294 (61.7%) were men. According to the age at admission, AMI patients were separated into group I ($\ge$65 years, n = 264) and group II (65 years, n = 212). The demographics, cardiovascular history, and risk factors of the two patient groups are shown in Table 1. Compared to group II, the group I patients were more often women (P 0.0001), less often current smokers (P 0.0001), with a history of systemic hypertension (P = 0.01), diabetes (P = 0.041), stroke (P = 0.02), congestive heart failure (P 0.002), and chronic kidney disease (P = 0.01). The values of serum creatinine and brain natriuretic peptide were higher in group I patients (P 0.0001, respectively P = 0.04). The elderly patients presented more often NSTEMI (P = 0.003), a higher functional class Killip (P 0.001), atrial fibrillation (P 0.001), 3rd atrioventricular block (P 0.0001), left ventricular ejection fraction 40% (P = 0.0002), and left ventricular diastolic dysfunction (P = 0.003).

Table 2 presents the data of emergency coronagraphy. No angiography could be done in 5 (1.9%) of group I patients and 2 (0.09%) patients of group II (P = 0.66), because of severe kidney failure. Group II patients had a significantly higher proportion of monovascular coronary disease (P = 0.0001), a significantly lower proportion of triple vessel disease (P = 0.03), and had a significantly higher rate of interventional revascularization by PCI (79% vs. 65%, (P = 0.0008). The rate of coronary artery bypass graft was 2.6% in group II and 2% in group I (P = 0.66). Regarding the concomitant medication, diuretics were more often administered in group I patients (P = 0.02).

The total all-cause mortality rate, including in-hospital and 1-year mortality, was 14.3% (n = 67). The number of deaths was 50 (18.9%) for group I and 17 (8%) for group II, P = 0.0004.

During the hospitalization for AMI, 53 patients (12.3%) died, 39 being from group I (20%), and 14 from group II (6%), P 0.0001. The cardiac causes of death (n = 44, 9.2%) were more frequent in group I patients (n = 32, 12%), P = 0.016, while the noncardiac causes had similar frequencies in the two groups (see Table 3, Fig. 1).

Fig. 1.

Kaplan-Meier curves for in-hospital mortality.

The relative risk for in-hospital death for Group I patients was 2.5 (95% CI 1.12–5.77), P = 0.001, and 0.39 for Group II patients (95% CI 0.17–0.88).

The multivariate logistic regression selected two parameters as independent predictors for in-hospital death. These parameters were age $\ge$65 years (P = 0.017, 95% CI 0.512–0.626) and Killip functional class (P 0.0001, 95% CI 0.738–0.835). When comparing the ROC curves for these parameters, the Killip class was a more powerful predictor (AUC = 0.786) than age $\ge$65 years (AUC = 0.569), P 0.0001 (Fig. 2).

Fig. 2.

Comparison of receiver operating characteristic (ROC) curves of independent variables predictive for in-hospital all-cause death risk.

423 AMI patients were discharged alive (88.8%). Group I patients received at discharge more often oral anticoagulants (P = 0.0003) and diuretics (P = 0.045). and less often beta-blockers (P = 0.04).

During the 1-year follow-up phase, further 14 patients died. The 1-year mortality was 3.3%, slightly higher in group I patients (4.8% vs. 1.5%, P = 0.05), with no notable differences among the causes of death (Table 3).

Throughout the 1-year follow-up phase, 22 patients (5.2%) were rehospitalized. The readmission rate was lower in group I patients, but the difference was not notable (P = 0.24). The causes of readmissions had similar frequencies in the two groups (Table 4).