Background: Pulmonary hypertension (PH) is an independent risk factor of increased morbidity and mortality in cardiac surgery patients (CS). The most common cause underlying PH is left ventricular (LV) diastolic dysfunction. This study aimed to evaluate the echocardiographic probability of PH in patients undergoing CS and its correlation with postoperative respiratory adverse events (RAE). Methods: The echocardiographic probability of PH and its correlation with LV diastolic dysfunction was assessed in 56 consecutive adult patients who were qualified for coronary artery bypass grafting (CABG). Later, the postoperative RAE (such as pneumonia, pulmonary congestion, or hypoxemia), the length of intensive care unit (ICU) treatment and mortality in groups with moderate or high (PH-m/h) and low (PH-l) probability of pulmonary hypertension were examined. Results: PH-m/h was observed in 29 patients, of whom 65.5 % had LV diastolic dysfunction stage II or III. A significantly higher occurrence of RAE was observed in the PH-m/h group as compared to the PH-l group. There were no differences between the PH-m/h and PH-l patient groups regarding the in-hospital length of stay or mortality. Conclusions: High or intermediate probability of PH is common in cardiac surgical patients with left ventricular diastolic dysfunction and correlates with respiratory adverse events.

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The decline in cardiac contractility due to damage or loss of cardiomyocytes is intensified by changes in the extracellular matrix leading to heart remodeling. An excessive matrix response in the ischemic cardiomyopathy may contribute to the elevated fibrotic compartment and diastolic dysfunction. Fibroproliferation is a defense response aimed at quickly closing the damaged area and maintaining tissue integrity. Balance in this process is of paramount importance, as the reduced post-infarction response causes scar thinning and more pronounced left ventricular remodeling, while excessive fibrosis leads to impairment of heart function. Under normal conditions, migration of progenitor cells to the lesion site occurs. These cells have the potential to differentiate into myocytes in vitro, but the changed micro-environment in the heart after infarction does not allow such differentiation. Stem cell transplantation affects the extracellular matrix remodeling and thus may facilitate the improvement of left ventricular function. Studies show that mesenchymal stem cell therapy after infarct reduces fibrosis. However, the authors did not specify whether they meant the reduction of scarring as a result of regeneration or changes in the matrix. Research is also necessary to rule out long-term negative effects of post-acute infarct stem cell therapy.