Despite aortic stenosis (AS) relief, patients undergoing transcatheter aortic valve implantation (TAVI) are at increased risk of developing heart failure (HF) within first months of intervention. Sodium-glucose co-transporter 2 (SGLT-2) inhibitors have been shown to reduce the risk of HF hospitalization in individuals with diabetes mellitus, reduced left ventricular ejection fraction and chronic kidney disease. However, the effect of SGLT-2 inhibitors on outcomes after TAVI is unknown. The Dapagliflozin after Transcatheter Aortic Valve Implantation (DapaTAVI) trial is designed to assess the clinical benefit and safety of the SGLT-2 inhibitor dapagliflozin in patients undergoing TAVI.
An 85-year-old man wearing a pacemaker because of previous history of atrial flutter with paroxysmal atrioventricular block was admitted presenting with syncope. Relevant past history included hypertension, rheumatoid arthritis, and a low-risk IgG kappa monoclonal gammopathy of uncertain significance. ECG at arrival showed an atrial fibrillation with spontaneously controlled ventricular rate (Figure 1). The pacemaker recorded multiple episodes of nonsustained ventricular tachycardia at 300 bpm. An echocardiogram showed concentric hypertrophy with enlarged atrium and mild pericardial effusion (Figure 2; Movies I through IV in the Data Supplement). Differential diagnosis included hypertensive, hypertrophic, and infiltrative cardiomyopathies. A coronary angiography showed no stenotic lesions. A cardiac magnetic resonance imaging showed concentric left ventricular hypertrophy with maximum thickness at the septum (16 mm) with a rapid washout of gadolinium after injection. A diffuse subendocardial enhancement and interatrial septum gadolinium uptake was observed. In the presence of conduction disorders in the ECG, these data suggested an infiltrative cardiomyopathy such as cardiac amyloidosis (CA; Figure 3). An abdominal fat biopsy and a bone marrow biopsy were negative for amyloid. A complete workup for systemic light-chain (AL) amyloidosis showed no signs of progression. Scintigraphy with 99-technetium-1,1-diphosphonopropane-2,3-dicarboxylic acid (Tc-99-DPD) showed an intense radiotracer uptake (grade 3 of Perugini) in the myocardial wall affecting both ventricles (Figure 4). DPD scintigraphy shows an intense radiotracer uptake (grade 3 of Perugini) in the left ventricle (Figure 4). A less marked uptake is also seen in the right ventricle. An endomyocardial biopsy was performed and showed deposition of amyloid material by Congo Red staining. Transthyretin amyloidosis (ATTR) was confirmed using immunohistochemistry (Figure 5). A genetic study was performed to distinguish between wild-type and hereditary forms of ATTR, and results were negative for hereditary forms. At the time of writing, the patient remains asymptomatic, with cessation of ventricular tachycardia with β-blockers.
Background
Microvascular obstruction (MVO) is a phenomenon that occurs frequently even after primary coronary intervention with recanalization of the infarct-related artery (IRA) and it has been shown to increase the risk of adverse cardiovascular events in ST-segment elevation myocardial infarction (STEMI) patients. The most important clinical predictor of MVO is ischemia duration, but there is a lack of information regarding predictor factors in promptly revascularized patients.
Methods
From January 2007 to October 2017, 987 patients with STEMI that underwent urgent coronary angiography were retrospectively enlisted. We included 321 patients that were revascularized in ≤3 hours from symptom onset. Clinical and angiographic data were taken from hospital records. A univariate and multivariate Cox regression analysis was made to assess the relationship between MVO (defined as final TIMI <3 in IRA) and potential predictors.
Results
From the 321 patients included, 76.9% were male and the mean age was 63.6±13.4 years. LVEF at admission was 46.2±12%. The mean time between symptom onset and wire crossing was 2.2±0.6 hours and MVO was found in 43 cases (13.4%). Descriptive data of predictor factors and their association with MVO are shown in Table 1. After the multivariate Cox regression analysis, smoking was a protector factor of MVO (OR 0.39 [0.16–0.96]). Age (OR 1.03 [1.01–1.06]) and Killip class III-IV at admission (OR 5.96 [2.1–16.4]) were directly associated with MVO. No other clinical variables were independently associated with the occurrence of MVO.
Conclusions
In very early presenters of STEMI, age and Killip class III-IV at admission were clinical predictor factors of MVO. Current smoking could carry a protector mechanism for MVO in this population, that is yet to be confirmed with prospective studies.
Funding Acknowledgement
Type of funding source: None
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