ABSTRACT
OBJECTIVE: Moderate to severe mitral regurgitation (MR) and tricuspid regurgitation (TR) are present in approximately 20-60% of patients undergoing transcatheter aortic valve implantation (TAVI). This study aims to evaluate the impact of TAVI on MR and TR, pulmonary hypertension, and reverse cardiac remodeling in these patients. Methods: Out of 240 patients who underwent TAVI, 79 who met the inclusion and exclusion criteria were analyzed. RESULTS: In our study, 46.8% (n = 37) of the patients were male. Nineteen (24.1%) patients died within two years. Before TAVI, 34 (43%) patients had moderate-to-severe MR, which decreased to 18 (22.7%) after the procedure (P < 0.05). Similarly, the number of patients with moderate-to-severe TR decreased from 26 (32.9%) before TAVI to 12 (15%) after the procedure (P < 0.05). Of the patients, 50.6% (n = 40) did not require hospitalization after the procedure, while 25 were hospitalized once, 12 twice, and 2 three times. The mean systolic pulmonary artery pressure (sPAP) values of the patients decreased from 44.30 ± 14.42 mmHg before the procedure to 39.09 ± 11.77 mmHg after the procedure (Z=-3.506, P < 0.001). No correlation was found between changes in MR and TR grades after TAVI and mortality or hospitalization during follow-up. Furthermore, there was no statistically significant difference in tricuspid annular plane systolic excursion (TAPSE), free wall annular S' velocity, left atrial volume (LAV), or LAV index (LAVI) before and after TAVI. Conclusion: There was a significant decrease in moderate-to-severe MR and TR after TAVI; however, this did not impact hospitalization or mortality rates. Additionally, no significant differences were observed in right ventricular systolic function or in LAV and LAVI before and after TAVI.
Subject(s)
Aortic Valve Stenosis , Heart Valve Prosthesis Implantation , Mitral Valve Insufficiency , Transcatheter Aortic Valve Replacement , Tricuspid Valve Insufficiency , Humans , Male , Female , Transcatheter Aortic Valve Replacement/methods , Tricuspid Valve Insufficiency/diagnostic imaging , Tricuspid Valve Insufficiency/epidemiology , Mitral Valve Insufficiency/epidemiology , Mitral Valve Insufficiency/surgery , Treatment Outcome , Heart Valve Prosthesis Implantation/adverse effects , Heart Valve Prosthesis Implantation/methods , Aortic Valve Stenosis/surgery , Aortic Valve/surgerySubject(s)
Computed Tomography Angiography/methods , Coronary Angiography/methods , Coronary Vessel Anomalies , Coronary Vessels , Pulmonary Artery , Vascular Malformations , Vascular Surgical Procedures/methods , Chest Pain/diagnosis , Chest Pain/etiology , Coronary Vessel Anomalies/diagnosis , Coronary Vessel Anomalies/surgery , Coronary Vessels/diagnostic imaging , Coronary Vessels/surgery , Humans , Male , Middle Aged , Pulmonary Artery/abnormalities , Pulmonary Artery/diagnostic imaging , Pulmonary Artery/surgery , Treatment Outcome , Vascular Malformations/diagnostic imaging , Vascular Malformations/physiopathology , Vascular Malformations/surgeryABSTRACT
BACKGROUND: Septal reduction therapy can be considered along the lines of hypertrophic obstructive cardiomyopathy patients who have drug-refractory symptoms. This can be applied either surgical myectomy or either alcohol septal ablation (ASA). Alcohol septal ablation has been performed successfully since the first announcement of ASA in 1995. CASE SUMMARY: We present a case report of coronary artery vasospasm that occurred in the left anterior descending artery (LAD) during ASA. We performed ASA via first septal artery. Two cubic centimetre of 99% ethanol was slowly injected and 10 min later balloon was withdrawn. Then the patient felt severe chest pain; his systolic blood pressure went down quickly and fibrillated. We started the cardiopulmonary resuscitation (CPR). After CPR, the rhythm was achieved total 4 min later cardiac arrest but blood pressure was low. Emergent coronary angiography showed that coronary spasm caused severe occlusion in the LAD segment just after the first septal artery and impaired coronary flow nearly totally in the LAD just after septal artery. At that time, we decided to implant a stent due to the patient's serious condition and a 3.5 × 18 mm drug-eluting stent was implanted. We performed control angiography to patient 3 days later of the procedure and LAD flow was TIMI 3. DISCUSSION: The causes of LAD occlusion are alcohol leakage, dissection, and vasospasm. It is important to detect the correct reason for appropriate treatment. Alcohol leakage impairs and causes coronary flow disruption; this can cause ventricular wall motion abnormalities. In our case, there was severe spasm in the LAD coronary artery and LAD flow was severely impaired. On echocardiogram, there was no myocardial wall motion abnormality. So alcohol leakage was ruled out. Left anterior descending artery image was not typical dissection. As a result of these findings, we concluded that the cause of LAD occlusion was coronary artery vasospasm.
