Cardiorenal syndrome signs in cats with thickened heart muscle

Abstract

This research presents novel insights into the temporal dynamics of clinical and instrumental parameters pertaining to the emergence of cardiorenal syndrome in feline patients afflicted with hypertrophic cardiomyopathy. It elucidates that within pedigreed felines, the progression of congestive heart failure syndrome may precipitate the subsequent evolution and exacerbation of secondary renal damage, thus significantly complicating the trajectory of the primary pathological process. This study establishes, for the first time, theprevalence of cardiorenal syndrome, affecting 51.0% of the population within the broader cohort of cats afflicted with hypertrophic cardiomyopathy (n= 49). Moreover, it substantiates the role of the cardiorenal continuum in felines as apredictor of amore severe course of hypertrophic cardiomyopathy. Manifesting as concentric myocardial hypertrophy in domestic felines, cardiorenal syndrome is characterized by dyspnea, hypothermia, and circulatory insufficiency. Statistically significant findings include an elevated median nocturnal respiratory rate of 34.0 breaths/min (p0.001) compared to clinically healthy counterparts (18.0 breaths/min) in affected felines. Additionally, felines afflicted with hypertrophic cardiomyopathy and cardiorenal syndrome exhibit astatistically significant (p 0.001) elevation in median mean arterial blood pressure to 140.0 mmHg compared to clinically healthy counterparts (104.0 mmHg), sinus tachycardia at 199.0 beats/min (171.5 beats/min in healthy felines), resulting in astatistically significant (p 0.001) reduction in PQ intervals by 67.0 ms (75.5 ms in healthy felines), and an increase in QT interval by 204.0 ms (165.5 ms in healthy felines). Electrocardiographic assessments reveal indications of compromised intra-atrial and intraventricular conduction in hypertrophic cardiomyopathy-afflicted felines with cardiorenal syndrome, along with an augmented amplitude of the ventricular complex. Echocardiographic evaluations confirm alterations such as pulmonary vein dilation, pronounced left atrial anteroposterior enlargement, interventricular septal and left ventricular free wall hypertrophy, decreased longitudinal contractility of the left and right ventricles, and clinically significant diastolic dysfunction.