Prevalence and Clinical Significance of Heart Murmurs Detected on Cardiac Auscultation in 856 Cats.

BACKGROUND: Cardiac auscultation is one of the most important clinical tools to identify patients with a potential heart disease. Although several publications have reported the prevalence of murmurs in cats, little information is available in relation to the exact origin of the blood flow turbulences responsible for these murmurs. The aim of this study was to determine the prevalence and clinical significance of murmurs detected during physical examination in cats. METHODS: Retrospective evaluation of clinical records and echocardiographic examinations performed in cats for investigation of heart murmurs; Results: Records of 856 cats with full clinical information were available for review. The cause of murmur was identified in 93.1% of cases (72.3% with single blood flow turbulence, 26.4% with two, and 1.3% with three identifiable sources of murmur). Systolic anterior motion of the mitral valve (SAM) was the primary cause of murmur in this population (39.2%), followed by dynamic right ventricular outflow tract obstruction (DRVOTO) (32%) and flow murmurs (6.9%). Most cats with a murmur (56.7%) did not present any structural cardiac abnormality. CONCLUSIONS: This study indicates that some heart murmur characteristics (timing, loudness and point of maximal intensity) can potentially predict the presence of an underlying cardiac disease.

Infection with SARS-CoV-2 variant B.1.1.7 detected in a group of dogs and cats with suspected myocarditis.

BACKGROUND: Domestic pets can contract severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection; however, it is unknown whether the UK B.1.1.7 variant can more easily infect certain animal species or increase the possibility of human-to-animal transmission. METHODS: This is a descriptive case series reporting SARS-CoV-2 B.1.1.7 variant infections in a group of dogs and cats with suspected myocarditis. RESULTS: The study describes the infection of domestic cats and dogs by the B.1.1.7 variant. Two cats and one dog were positive to SARS-CoV-2 PCR on rectal swab, and two cats and one dog were found to have SARS-CoV-2 antibodies 2-6 weeks after they developed signs of cardiac disease. Many owners of these pets had developed respiratory symptoms 3-6 weeks before their pets became ill and had also tested positive for COVID-19. Interestingly, all these pets were referred for acute onset of cardiac disease, including severe myocardial disorders of suspected inflammatory origin but without primary respiratory signs. CONCLUSIONS: These findings demonstrate, for the first time, the ability for pets to be infected by the B.1.1.7 variant and question its possible pathogenicity in these animals.

Heart murmurs in apparently healthy cats caused by iatrogenic dynamic right ventricular outflow tract obstruction.

BACKGROUND: Heart murmurs are detected commonly in apparently healthy cats during routine physical examination, and Doppler echocardiography ultimately is required to identify the source of flow turbulence causing the murmur. However, in some cases, the origin of the murmur cannot be identified on echocardiographic examination, even by experienced clinicians. The application of gentle pressure with the ultrasound transducer against the chest wall of a cat can induce temporary narrowing of the mid-right ventricular (RV) lumen, causing blood flow turbulence even in the absence of cardiac abnormalities. OBJECTIVES/HYPOTHESES: To evaluate the effect of pressure of the ultrasound transducer against the chest wall of cats during echocardiography (provocative testing) on RV blood flow. The main hypothesis is that provocative testing can increase RV outflow velocity and cause flow turbulence. The second hypothesis is that the effect of this maneuver is independent of changes in heart rate during testing. ANIMALS: Sixty-one client-owned, apparently healthy cats with heart murmurs on physical examination. METHODS: Retrospective review of echocardiographic examinations of 723 cats presented for investigation of a heart murmur. RESULTS: Outflow systolic velocity increased from 1.05 ± 0.26 to 1.94 ± 0.51 m/s during provocative testing (P < .0001); no correlation was found between RV outflow peak velocity and heart rate during provocative testing (P = .34; r = 0.1237). CONCLUSIONS AND CLINICAL RELEVANCE: Right ventricular outflow tract obstruction and associated heart murmur can be iatrogenically induced in apparently healthy cats by increasing pressure on the right chest wall with an ultrasound probe.

Haemodynamic changes during propofol induction in dogs: new findings and approach of monitoring.

BACKGROUND: Propofol is one of the most widely used injectable anaesthetic agents in veterinary practice. Cardiovascular effects related to propofol use in dogs remain less well defined. The main objective of this study was to evaluate the haemodynamic changes during induction of general anaesthesia with propofol in healthy dogs, by a beat-to-beat continuous monitoring. All dogs were premedicated with intramuscular acepromazine (0.015 mg/kg) and methadone (0.15 mg/kg). Transthoracic echocardiography was used to measure the velocity time integral (VTI) of the left ventricular outflow tract. A syringe driver, programmed to deliver propofol 5 mg/kg over 30 s followed by a continuous infusion of 25 mg/kg/h, was used to induce and maintain anaesthesia. From the initiation of propofol administration, heart rate (HR) and mean invasive arterial blood pressure (MAP) were recorded every 5 s for 300 s, while aortic blood flow was continuously recorded and stored for 300 S. maximum cardiovascular depression was defined the lowest MAP (MAP_Tpeak) recorded during the monitored interval. VTI and VTI*HR were calculated at 0, 30, 90, 120, 150 and 300 s post administration of propofol, and at MAP_Tpeak. Haemodynamic effects of propofol in relation to plasma and biophase concentrations were also evaluated by pharmacokinetics simulation. RESULTS: The median (range) HR was significantly higher (p = 0.006) at the moment of maximum hemodynamic depression (Tpeak) [105(70-148) bpm] compared with pre-induction values (T0) [65(50-120) bpm]. The median (range) MAP was significantly lower (p < 0.001) at Tpeak [61(51-69) mmHg] compared with T0 [88(72-97) mmHg]. The median (range) VTI and VTI*HR were similar at the two time points [11.9(8.1-17.3) vs 13,3(9,4-16,5) cm, and 1172(806-1554) vs 1002(630-1159) cm*bpm, respectively]. CONCLUSIONS: Induction of anaesthesia with propofol causes a drop of arterial pressure in healthy dogs, however cardiac output is well maintained by compensatory chronotropic response. The magnitude of MAP_Tpeak may be strictly related with propofol plasma concentration.