Increased sensitivity of prolonged P-wave during exercise stress test in detection of angiographically documented coronary artery disease

Background: A retrospective study was designed to investigate P-wave duration changes in exercise stress test (EST) for the prediction of angiographically documented substantial coronary artery disease (CAD). Methods: We analyzed 265 cases of patients, who underwent EST and subsequently coronary angiography. Analysis of P-wave duration was performed in leads II, V5 at rest, and in the recovery period. Results: The sensitivity and specificity for the isolated ST-segment depression were only 31% and 76%, respectively. The combination of ST-depression with other exercise-induced clinical and electrocardio­graphic abnormalities (chest pain, ventricular arrhythmia, hypotension, left bundle branch block) was characterized by 41% sensitivity and 69% specificity. The combination of abnormal recovery P-wave duration (≥ 120 ms) with ST-depression and other exercise-induced abnormalities had 83% sensitivity but only 20% specificity. Combined analysis of increased delta P-wave duration, ST-depression and other exercise-induced abnormalities had 69% sensitivity and 42% specificity. Sensitivity and specificity of the increase in delta P-wave duration for left CAD was 69% and 47%, respectively, and for 3-vessel CAD 70% and 50%, respectively. The presence of arterial hypertension negatively influenced the prog­nostic value of P-wave changes in the stress test. Conclusions: The results of the study show that an addition of P-wave duration changes assessment to ST-depression analysis and other exercise-induced abnormalities increase sensitivity of EST, especially for left CAD and 3-vessel coronary disease. We have also provided evidence for the negative influence of the presence of arterial hypertension on the predictive value of P-wave changes in the stress test. (Cardiol J 2017; 24, 2: 159–166

Increased Activity of the Intracardiac Oxytocinergic System in the Development of Postinfarction Heart Failure

Aim. The present study was designed to test the hypothesis that the development of postinfarction heart failure is associated with a change of activity of the intracardiac oxytocinergic system. Methods. Experiments were performed on male Sprague-Dawley rats subjected to myocardial infarction or sham surgery. Four weeks after the surgery, blood samples were collected and the samples of the left ventricle (LV) and right ventricle (RV) were harvested for evaluation of the mRNA expression (RT-PCR) of oxytocin (OT), oxytocin receptor (OTR), natriuretic peptides, and the level of OT and OTR protein (ELISA). The concentration of N-terminal B-type natriuretic peptide was measured to determine the presence of heart failure. Results. Plasma NT-proBNP concentration was higher in the infarcted rats. In the infarcted rats, the expression of OT mRNA and the OT protein level were higher in the RV. There were no significant differences between infarcted and noninfarcted rats in the expression of OT mRNA and in the OT protein level in the fragments of the LV. In both the left and the right ventricles, OTR mRNA expression was lower but the level of OTR protein was higher in the infarcted rats. Conclusions. In the present study, we indicate that postinfarction heart failure is associated with an increased activity of the intracardiac oxytocinergic system

Complementary Role of Oxytocin and Vasopressin in Cardiovascular Regulation

The neurons secreting oxytocin (OXY) and vasopressin (AVP) are located mainly in the supraoptic, paraventricular, and suprachiasmatic nucleus of the brain. Oxytocinergic and vasopressinergic projections reach several regions of the brain and the spinal cord. Both peptides are released from axons, soma, and dendrites and modulate the excitability of other neuroregulatory pathways. The synthesis and action of OXY and AVP in the peripheral organs (eye, heart, gastrointestinal system) is being investigated. The secretion of OXY and AVP is influenced by changes in body fluid osmolality, blood volume, blood pressure, hypoxia, and stress. Vasopressin interacts with three subtypes of receptors: V1aR, V1bR, and V2R whereas oxytocin activates its own OXTR and V1aR receptors. AVP and OXY receptors are present in several regions of the brain (cortex, hypothalamus, pons, medulla, and cerebellum) and in the peripheral organs (heart, lungs, carotid bodies, kidneys, adrenal glands, pancreas, gastrointestinal tract, ovaries, uterus, thymus). Hypertension, myocardial infarction, and coexisting factors, such as pain and stress, have a significant impact on the secretion of oxytocin and vasopressin and on the expression of their receptors. The inappropriate regulation of oxytocin and vasopressin secretion during ischemia, hypoxia/hypercapnia, inflammation, pain, and stress may play a significant role in the pathogenesis of cardiovascular diseases

Evaluation and Comparison of the STIMUL Extended and Simplified Risk Scores for Predicting Two-Year Death in Patients Following ST-Segment Elevation Myocardial Infarction

Background and Objectives: The management of ST-segment elevation myocardial infarction (STEMI) requires a patient’s long-term risk to be estimated. The objective of this study was to develop extended and simplified models of two-year death risk estimation following STEMI that include and exclude cardiac troponins as prognostic factors and to compare their performance with each other. Materials and Methods: Extended and simplified multivariable logistic regression models were elaborated using 1103 patients with STEMI enrolled and followed up in the STIMUL (ST-segment elevation Myocardial Infarctions in Ukraine and their Lethality) registry. Results: The extended STIMUL risk score includes seven independent risk factors: age; Killip class ≥ II at admission; resuscitated cardiac arrest; non-reperfused infarct-related artery; troponin I ≥ 150.0 ng/L; diabetes mellitus; and history of congestive heart failure. The exclusion of cardiac troponin in the simplified model did not influence the predictive value of each factor. Both models divide patients into low, moderate, and high risk groups with a C-statistic of 0.89 (95% CI 0.84–0.93; p < 0.001) for the extended STIMUL model and a C-statistic of 0.86 (95% CI 0.83–0.99; p < 0.001) for the simplified model. However, the addition of the level of troponin I to the model increased its prognostic value by 10.7%. Conclusions: The STIMUL extended and simplified risk estimation models perform well in the prediction of two-year death risk following STEMI. The simplified version may be useful when clinicians do not know the value of cardiac troponins among the population of STEMI patients