We studied the expression and distribution of atrial natriuretic polypeptide in the ventricles of 27 autopsied children with Kawasaki disease. Fourteen of the children had died in the acute stage of the disease. Three without any coronary artery aneurysms died due to myocarditis, while 11 with coronary artery aneurysms also had myocarditis but died of coronary heart disease. Histologic evidence of acute myocardial infarction was noted in three children who died of coronary heart disease. In the 14 children with acute-stage deaths, no abnormal expression of atrial natriuretic polypeptide was noted in the ventricles, despite the presence of heart failure in seven of them for 2 to 22 days before death. The other 13 patients had coronary artery aneurysms and died in the healed stage. In three patients with granulation tissue and congestive heart failure, myocytes in foci around the granulations were moderate to markedly positive for atrial natriuretic polypeptide. These three patients died over 8 days after the onset of their first myocardial infarct. Of 10 patients with old myocardial infarction, four had a history of congestive heart failure. They demonstrated moderate or marked atrial natriuretic polypeptide expression in extensive regions around sites of massive fibrosis, and foci of slight expression in the inner third of the noninfarcted region of the ventricle. In the other six patients without congestive heart failure, there was slight or moderate expression in foci around sites of massive fibrosis. We concluded that the expression of atrial natriuretic polypeptide appeared more than 1 week after the onset of acute myocardial infarction in the ventricles of children with Kawasaki disease who died in the healed stage.(ABSTRACT TRUNCATED AT 250 WORDS)
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/0002-8703(90)90019-t | DOI Listing |
Orphanet J Rare Dis
January 2025
Department of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, 6-1 Kishibe-Shimmachi, Suita, Osaka, 564-8565, Japan.
Background: Transient receptor potential cation channel subfamily V member 2 (TRPV2) functions as a stretch-sensitive calcium channel, with overexpression in the sarcolemma of skeletal and cardiac myocytes leading to detrimental calcium influx and triggering muscle degeneration. In our previous pilot study, we showed that tranilast, a TRPV2 inhibitor, reduced brain natriuretic peptide levels in two patients with muscular dystrophy and advanced heart failure. Building on this, we performed a single-arm, open-label, multicenter study herein to evaluate the safety and efficacy of tranilast in the treatment of advanced heart failure in patients with muscular dystrophy.
View Article and Find Full Text PDFJ Cardiol
January 2025
Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, China; Kent and Medway Medical School, Canterbury, Kent, UK; School of Nursing and Health Studies, Hong Kong Metropolitan University, Hong Kong, China.
Approximately 10 % of patients who have suffered from myocardial infarction develop new-onset atrial fibrillation (AF). Coronary artery disease implicating atrial branches has been associated with AF. The following variables have been associated with new-onset AF in the setting of acute coronary syndrome: older age, history of hypertension, history of angina, history of stroke, chronic renal failure, body mass index, no statin use, worse nutritional status, worse Killip class, admission heart rate ≥ 85 bpm, complete atrioventricular block, Glasgow prognostic score, Syntax score, CHEST score > 3, PRECISE-DAPT score ≥ 25, left ventricular ejection fraction ≤40 %, increased left atrial diameter, E/E' ratio > 12, epicardial fat tissue thickness, and thrombolysis in myocardial infarction flow <3.
View Article and Find Full Text PDFInt J Med Sci
January 2025
Department of Cardiology, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, People's Republic of China.
The efficacy of radiofrequency ablation (RFA) in patients with atrial fibrillation (AF) and heart failure with preserved ejection fraction (HFpEF) has been established, but the efficacy and safety of cryoballoon ablation (CBA) and pulsed field ablation (PFA) remain unclear. This retrospective cohort study included 223 patients with paroxysmal non-valvular AF and HFpEF who underwent their first AF ablation between January 2017 and December 2021 and were divided into RFA (n = 77), CBA (n = 127), and PFA (n = 19) groups. After a mean follow-up of 11.
View Article and Find Full Text PDFBiomarkers
January 2025
Department of Cardiology, The Heart Centre, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Background: The Thrombolysis in Myocardial Infarction (TIMI) risk score estimates mortality for patients with ST-elevation myocardial infarction (STEMI). This study aimed to investigate whether biomarkers reflecting the neurohormonal response (pro-atrial natriuretic peptide (proANP), mid-regional pro-adrenomedullin (MR-proADM), and copeptin), inflammation (suppression of tumorigenicity 2 (ST2), C-reactive protein (CRP), and leukocytes), and troponin add prognostic value to the TIMI risk score.
Methods: This sub-study of the prospective PREDICT cohort included 1700 non-comatose and non-cardiogenic shock STEMI patients upon admission.
Medicina (Kaunas)
November 2024
Department of Microbiology, "Victor Babes" University of Medicine and Pharmacy, 300041 Timisoara, Romania.
: Heart failure is associated with high morbidity and mortality and linked with several pre-existing health conditions and risk factors. Early detection and prompt management in heart failure improves patient outcomes. Liver involvement is associated with heart failure disease progression, and hence liver biomarkers and liver fibrosis may have a prognostic impact.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!