These results indicate that coronary perivascular fibrosis is associated with the impairment of coronary blood flow although not associated with interstitial fibrosis or cardiac function, suggesting that it can be a new therapeutic target to improve coronary microcirculation.

No abstract

Pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension which occurs in 0.1-0.2 people per million. Its etiology is still poorly understood but is related to several risk factors. The histopathology of PVOD is characterized by intimal fibrosis narrowing or the occlusion of small pulmonary veins or venules. A definitive diagnosis requires a surgical biopsy, which is a risky procedure. Thus, the diagnosis must be based on high clinical suspicion and the results of various diagnostic tests, mainly high-resolution computed tomography, pulmonary function tests, bronchoalveolar lavage, and right heart catheterization. The definitive treatment is limited to lung transplantation. Several pulmonary arterial hypertension-specific agents may cause pulmonary edema in PVOD. However, the cautious use of such medications in selected patients, and surgical or mechanical supports, may successfully bridge patients to transplantation. Given the scant knowledge regarding this entity, future studies with a focus on elucidating the etiology and establishing the optimal treatment are required, as is further development in diagnosis.

No abstract

The underlying mechanisms of ventricular remodeling after myocardial infarction (MI) remain largely unknown. In this study, we performed an integrative analysis of spatial transcriptomics and single-nucleus RNA sequencing (snRNA-seq) in a murine MI model and found that mechanical stress-response genes are expressed at the border zone and play a critical role in left ventricular remodeling after MI. An integrative analysis of snRNA-seq and spatial transcriptome of the heart tissue after MI identified the unique cluster that appeared at the border zone in an early stage, highly expressing mechano-sensing genes, such as Csrp3. AAV9-mediated gene silencing and overexpression of Csrp3 demonstrated that upregulation of Csrp3 plays critical roles in preventing cardiac remodeling after MI by regulation of genes associated with mechano-sensing. Overall, our study not only provides an insight into spatiotemporal molecular changes after MI but also highlights that the mechano-sensing genes at the border zone act as adaptive regulators of left ventricular remodeling.

No abstract

Background: N-terminal pro-B-type natriuretic peptide (NT-proBNP) is a potential biomarker for monitoring the status of heart failure. However, the optimal monitoring interval of NT-proBNP is unknown. This study sought to investigate the minimal informative monitoring interval of NT-proBNP in patients with stable chronic heart failure. Methods: This retrospective cohort study included patients who were admitted due to heart failure and subsequently followed with serial NT-proBNP measurements in a tertiary hospital. We analyzed NT-proBNP measured between six months after discharge and the earliest timepoint of: an alteration of medication regimen, readmission due to worsening of heart failure, or all-cause death. To distinguish progression of the disease from biological variability and measurement error, the signal-to-noise ratio method was applied with a random-effects model. Results: In the 368 patients included, NT-proBNP was measured for a median 6 times. In the random-effects model, signal (progression of disease) exceeded noise (biological variability and measurement error) at 7.9 months (95% confidence interval [CI]: 5.1-9.6), while noise corresponded to a 61% increase from baseline. In stratified analysis using the AHEAD risk score, the minimal informative monitoring interval shortened as the risk score increased (0-1

Sodium-glucose cotransporter-2 (SGLT2) inhibitors are a new class of antidiabetic drug that have pleiotropic effects including improving cardiovascular outcomes [1]. Medicines of this class are known to have several adverse effects, including euglycemic diabetic ketoacidosis (DKA), which has been reported increasingly [2]. Here, we report a case of SGLT2 inhibitor-associated euglycemic DKA that was complicated with cardiac arrest from acute myocardial infarction. Case report A 49-year-old Asian man with a 1-year history of type 2 diabetes mellitus and vasospastic angina, whose body mass index was 22.1 kg/m 2 , suddenly lost consciousness while sightseeing, shortly after he complained of nausea. An automated external defibrillator was initiated 5 min later, without bystander cardiopulmonary resuscitation. On the basis of initial cardiac rhythm of ventricular fibrillation, the automated external defibrillator delivered 2 shocks. The emergency medical service arrived and started basic life support, and delivered 4 shocks. Return of spontaneous circulation was achieved after a total resuscitation time of 16 min. He was rushed to the emergency department (ED) of our hospital while unconscious. Upon arrival at the ED, his Glasgow coma scale was E1V2M2. His blood pressure was 136/90 mmHg and heart rate was 85 beats/ min. His respiration rate was 20 breaths/min, and peripheral oxygen saturation was 100% on 100% oxygen delivery. His initial 12-lead electrocardiograms showed ST-segment elevation in precordial leads, I, and aVL and reciprocal ST-segment depression in III and aVF (Fig. 1A). A transthoracic echocardiography demonstrated hypokinesis of basal to apical left ventricular (LV) anteroseptal wall. We, therefore, diagnosed him as having acute anteroseptal myocardial infarction. After intubation and a brain computed tomography ruling out an intracranial event, we initiated targeted temperature (34 8C) management (TTM). Emergency coronary angiography revealed a subtotal stenosis in proximal left anterior descending (LAD) artery under nitrate administration (Fig. 1B), which was most likely to be organic stenosis. We did not utilize intravascular imaging modalities, in