The importance of ST elevation in V2-4 ECG leads in athletes.

BACKGROUND: Early repolarization in the anterior ECG leads (ERV2-4) is considered to be a sign of right ventricular (RV) remodeling, but its etiology and importance are unclear. METHODS: A total of 243 top-level endurance-trained athletes (ETA; 183 men and 60 women, weekly training hours: 15-20) and 120 leisure-time athletes (LTA; 71 men and 49 women, weekly training hours: 5-6) were investigated. The ERV2-4 sign was evaluated concerning type of sport, gender, transthoracic echocardiographic parameters, and ECG changes, which can indicate elevated RV systolic pressure [left atrium enlargement (LAE), right atrium enlargement (RAE), RV conduction defect (RVcd)]. RESULTS: Stroke volume and left ventricular mass were higher in ETAs vs. LTAs in both genders (p < 0.01). Prevalence of the ERV2-4 sign was significantly higher in men than in women [p = 0.000, odds ratio (OR) = 36.4] and in ETAs than in LTAs (p = 0.000). The highest ERV2-4 prevalence appeared in the most highly trained triathlonists and canoe and kayak paddlers (OR = 13.8 and 5.2, respectively). Within the ETA group, the post-exercise LAE, RAE, and RVcd changes developed more frequently in cases with than without ERV2-4 (LAE: men: p < 0.05, females: p < 0.005; RAE: men: p < 0.05, females: p < 0.005; RVcd: N.S.). These post-exercise appearing LAE, RAE, and RVcd are associated with the ERV2-4 sign (OR = 4.0, 3.7, and 3.8, respectively). CONCLUSIONS: According to these results, ERV2-4 develops mainly in male ETAs due to long-lasting and repeated endurance training. The ERV2-4 sign indicates RV's adaptation to maintain higher compensatory pulmonary pressure and flow during exercise but its danger regarding malignant arrhythmias is unclear.

Non-ST elevation myocardial infarction: a new pathophysiological concept could solve the contradiction between accepted cause and clinical observations.

UNLABELLED: Non-ST elevation myocardial infarction (NSTEMI) and ST elevation infarction have many differences in their appearance and prognosis. A comprehensive search made us form a new hypothesis that a further cause also existsin NSTEMI: an acute, critical increase in the already existing high microvascular resistance in addition to the subtotal coronary artery occlusion. Various findings and studies can be interpreted only by our hypothesis: hemodynamic findings, ECG changes, autopsy reports and clinical observations (different long-time prognosis and different result of acute revascularization therapy in NSTEMI, similarities of NSTEMI with other clinical symptoms where increased microvascular resistance can be supposed without coronary artery disease). OBJECTIVE: Despite similarities in the underlying pathologic mechanism non-ST elevation myocardial infarction(NSTEMI) and ST elevation infarction (STEMI) have many differences in their clinical presentation and prognosis. METHOD: A systematic review of the literature about NSTEMI and the blood supply of the myocardium made us form a hypothesis that a further cause also exists in addition to the accepted cause of NSTEMI (subtotal coronaryartery occlusion): an acute, critical increase in an already existing high intramyocardial microvascular resistance. EVIDENCE: Knowledge about microcirculation disturbances in ischemic heart disease and development of microcirculation damage can be fitted in our hypothesis. Various findings and studies can be interpreted only by our hypothesis: hemodynamic findings, ECG changes, autopsy reports and clinical observations about NSTEMI. The latest ones involve the different long-time prognosis and different result of acute revascularization therapy in STEMI and NSTEMI. Regarding the repolarization changes on the ECG NSTEMI shows similarities with other clinical symptoms where increased intramyocardial microvascular resistance can be supposed without coronary artery disease: false positive exercise stress test, supraventricular tachycardia, left ventricular strain and conduction disturbances. CONCLUSION: The acute treatment of NSTEMI should aim to improve the blood inflow to the stiff myocardiumand/or impaired microvascular system and decrease the high microvascular resistance.