Clinical and demographic data of the study population are presented in Table 1. The vast majority of patients were men with pre-existing arterial hypertension, angina pectoris, and heart failure. Patients with anterior MI, multivessel coronary artery disease, and Killip II prevailed,  81.2% of patients underwent the revascularization of the infarct-related artery.

Table 1: Clinical and demographic data of the study cohort

The interventional neurologist reported that 20.9% (group 1) of patients had emotional lability, anxiety, phobias, slight reflex instability, and incoordination corresponding to mild encephalopathy. 67.6% of patients (group 2) had complaints about decreased memory and mental abilities, increased fatigue and decreased performance, emotional lability, headache, dizziness, sleep disturbance). Group 2 patients had mild neurological disorders corresponding to moderate encephalopathy. 11.5% of patients (group 3) had a positive history of ischemic stroke. The severity of cognitive deficit measured with the MMSE corresponded to the severity of encephalopathy: group 1 - 25 (24; 27) points (pre-dementia), group 2 - 25 (24; 26) points (pre-dementia), and group 3 - 23.5 (21; 25) points (mild dementia) (p2-3 = 0.006, p1-3 = 0.017).

According to the echocardiography and ultrasonography findings, all patients reported carotid intima-media thickness arteriopathy of >1 mm (the mean carotid intima-media thickness was 1.8±06 mm). 37.4% of patients had carotid atherosclerotic plaques. The severity of stenosis did not exceed 50% in all cases (Table 2).

aIMT – intima-media thickness

Тable 2: Carotid atherosclerotic lesions in the study cohort, n (%)

Five (2.7%) patients died due to recurrent myocardial infarction during the hospitalization. Thus, clinical data of 177 (91.7%) patients were used to predict the one-year prognosis.

Patients demonstrated high adherence to medical therapy within the year. 87% of patients continued to receive ACEI or ARB. 96% regularly took beta-blockers, 70% - diuretics, 64% - double antiplatelet therapy, and 63% - statins.

77 (43.5%) patients reached the hard endpoints within one year after MI. A total of 141 hard endpoints were collected, including 11 deaths, 52 cases of ACS, of them 22 recurrent MI and 30 cases of unstable angina, 8 ischemic strokes, and 31 cases of acute decompensated chronic heart failure. 19 patients underwent percutaneous coronary intervention with stenting and 20 patients were referred to coronary artery bypass grafting within the folreduced-up period.

Univariate regression reported that a history of stroke and carotid atherosclerotic plaques in the acute MI phase were the most significant individual risk factors associated with one-year mortality (Table 3).

aIRA – infarct-related artery

Table 3: Univariate regression analysis of the association of clinical and demographic data with one-year mortality, n (%)

Multivariate logistic regression reported prior stroke was the most unfavorable predictor of death within one year after MI (RR 7.33 [95% CI 1.97-27.32], p = 0.003).

We then performed univariate regression to determine the most likely predictors of adverse outcomes associated with the development of cardiovascular events in patients who reached hard endpoints and those who did not (Table 4)

aIRA – infarct-related artery

Table 4: Univariate regression analysis of the association of clinical and demographic data with a risk of cardiovascular events, n (%)

The risk factors associated with the development of cardiovascular events within the folreduced-up included the presence of carotid atherosclerotic plaques confirmed during the hospitalization and a positive history of stroke. Percutaneous coronary intervention (PCI) of the infarct-related artery was associated with a favorable prognosis.

Similar results were demonstrated by multivariate regression models. A positive history of stroke (RR = 1.92 [95% CI 1.09-3.38], p = 0.025) and the presence of carotid atherosclerotic plaque (RR = 2.12 [95% CI 1.34-3.37], p = 0.001) were the most significant predictors of adverse one-year annual prognosis. PCI of the infarct-related artery significantly improved one-year prognosis (RR = 0.6 [95% CI 0.38-0.95], p = 0.03).

Risk assessment of developing an adverse prognosis is crucial for understanding the medical and social significance of the disease and determining the intensity of subsequent treatment and secondary prevention. However, there are very few studies describing the effects of concomitant chronic cerebral ischemia on the prognosis after MI.

Systolic dysfunction developing after MI in patients with pre-existing carotid stenosis worsens chronic cerebral ischemia due to both, cardioembolic risk and hypoperfusion aggravation [18]. However, recent studies showed that the presence of significant brachiocephalic stenosis is not necessary in this case [21]. The presence of heart failure is known to contribute to the emergence or aggravation of autonomic, cognitive, and neuropsychological deficits due to a decrease in the thickness of the cerebral cortex, regardless of carotid stenosis [22]. A regional decrease in cerebral blood freduced occurs in patients with heart failure. This decrease is particularly pronounced in those patients who have pre-existing cerebral ischemia [23]. However, there is no clear relationship of the presence and severity of carotid stenosis and with the clinical manifestations of cerebral ischemia in patients with heart failure [21-23]. No doubt, the interaction between the damaged myocardium and altered cerebral functions in chronic cerebral ischemia affects the prognosis. Non-stenotic cerebral atherosclerosis in its turn can further worsen the prognosis in patients after myocardial infarction due to the risk of cerebral atherothrombotic events [19].

We found that carotid intima-media thickening was the main manifestation of carotid artery arteriopathy. The prevalence of carotid atherosclerotic plaques was reduced. The one-year mortality rate was 6.2% in the study group. Complete myocardial revascularization and optimal drug therapy in most patients resulted in improved survival. Logistic regression analysis showed the high significance of cerebral atherosclerosis, in particular, the presence of carotid atherosclerotic plaque and prior stroke contributed greatly to one-year prognosis in patients with CCI after MI. The onset of acute coronary syndrome is 

accompanied by morphological changes in atherosclerotic plaques and other vascular areas. This argument is confirmed by the ultrasonography findings reporting carotid plaque heterogeneity in the internal carotid arteries, their transition to an unstable state, “activation” in half of the patients several days after MI [14]. This transition from stable plaques to unstable plaques confirms the presence of common pathological mechanisms contributing to the development of adverse events. Our findings suggest that cerebral vascular events were more significant for long-term prognosis than reduced LVEF in patients with chronic cerebral ischemia.

Our findings are consistent with the results of the prospective CAFES-CAVE study suggesting the presence of a significant relationship between carotid atherosclerotic lesions and the incidence of cardiac complications [24]. Thus, the presence of even non-stenotic carotid atherosclerotic plaques significantly increased the risk of adverse cardiovascular events [24]. Thus, chronic cerebral perfusion can be considered as an additional extracardiac factor contributing to poor prognosis in patients with reduced LVEF after MI, including the risk of stroke. Large-scale studies showed that progressive impairment of left ventricular systolic function is associated with a 4-fold increase in the risk of stroke [25].

The presence of carotid atherosclerotic plaques and previous stroke affect the long-term prognosis in patients with chronic cerebral ischemia after myocardial infarction, complicated by heart failure. Our findings necessitate the development of target multidisciplinary approaches in secondary prevention and outpatient monitoring of patients with reduced left ventricular ejection fraction and concomitant chronic cerebral ischemia.

Ethics approval and consent to participate

Written informed consent was obtained from each patient. The study was approved by the Joint Local Ethics Committee of the Kemerovo Cardiological Dispensary and Federal State Budgetary Institution “Research Institute for Complex Issues of Cardiovascular Diseases” (Protocol No. 50 issued on 25.01.10).

Not applicable

Availability of data and materials

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request

The Authors declare that there is no сompeting of interest.

The study was funded bythe Ministry of Science and Higher Education (project No. 0546-2019-0003 “Atherosclerosis and Comorbidities. Diagnosis and risk management in a large Siberian industrial region”).

Lebedeva N.B. developed the concept and design of the study, contributed to the analysis, interpretation and synthesis of the data obtained, approved the final version of the article before submitting it for publication;

Chesnokova L.Yu. made a significant contribution to the receipt of data, their analysis and interpretation, wrote the first version of the article

Acknowledgements/ Not applicable

Lebedeva N.B. developed the concept and design of the study, contributed to the analysis, interpretation and synthesis of the data obtained, approved the final version of the article before submitting it for publication;

Chesnokova L.Yu. made a significant contribution to the receipt of data, their analysis and interpretation, wrote the first version of the article

Acknowledgements/ Not applicable