Connective tissue dysplasia (CTD) occurs in 70% of the patients with obstructive bronchial pathology. It promotes the development of electrical instability of myocardium and life-threatening arrhythmias. We studied electrocardiographic markers of myocardial instability in patients with chronic obstructive bronchial pathology and CTD markers. Such patients were shown to more frequently have ventricular and supraventricular arrhythmias, decreased circadian heart rate index and enhanced heart rhythm variability. Other findings included high frequency of such predictors of sudden cardiovascular death as prolonged and enhanced dispersion of QT intervals, T-wave microalternation, late atrial and ventricular potentials. The arrhythmic activity and the occurrence ofpredictors of sudden cardiovascular death increased in the patients aged above 60 years with obstructive bronchial pathology and CTD.
Aim. To characterize the remodeling of brachiocephalic arteries in patients with instable angina, taking into account morphological type. Materials and methods. Duplex scanning of brachiocephalic arteries was performed in 66 patients with instable angina and 59 practically healthy persons, comparable by sex and age. Results. It was established that in patients with instable angina remodeling of the vessels of brachiocephalic region occurs earlier, than in healthy persons, and diameter of the vessels of elastic type is changed to a greater degree. Remodeling of diameters is associated with the elevation of pumping ability of the heart. IMC of the vessels of combined and muscular types of brachiocephalic region in patients is essentially larger already by the age of 40 and grows with age. Conclusions. Hardness of the wall of brachiocephalic arteries of all types is higher in patients, than in healthy persons and grows with aging, with increase in pulse and systolic pressure, dyslipidemia.
The article presents a case report of spontaneous coronary artery dissection (SCAD) in the young woman with signs of undifferentiated connective tissue dysplasia (UCTD). The patient was admitted urgently with a clinical and electrocardiographic signs of acute ST-segment elevation coronary syndrome. The patient underwent a coronary angiography, which revealed a type D linear intimal dissection. The decision was made to perform balloon vasodilation with the placement of a drug-eluting stent. With multicomponent therapy, the patient’s condition improved. Physical examination revealed external markers of UCTD. Therefore, it was quantified by systems and organs. The patient had no other cardiovascular diseases, previous infection, or other trigger factors. She was discharged with recommendations to continue the prescribed therapy. This case report demonstrates SCAD as a rare cause of acute myocardial infarction in a young patient. The background for SCAD development in this case was UCTD. Algorithms for managing patients with SCAD against the background of UCTD have not been defined and require further study.
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