Capnocytophaga canimorsus and infective endocarditis-making a dog's dinner of the aortic valve: a case report.

BACKGROUND: Capnocytophaga canimorsus, a bacterium found in the oral cavities of healthy cats and dogs, is rarely reported as a cause of infective endocarditis. In this report we describe such a case in a young, male dog owner who presented acutely unwell in heart failure. CASE SUMMARY: A 47-year-old male presented with a subacute onset of fever, night sweats, weight loss, dyspnoea, and peripheral oedema. On clinical examination typical features of infective endocarditis, heart failure, and aortic regurgitation were found. The patient had no conventional risk factors for infective endocarditis but was a dog owner. Transthoracic echocardiography revealed vegetations on the right coronary and non-coronary cusps of the aortic valve causing severe eccentric aortic regurgitation and left ventricular dilatation. Initial blood cultures taken prior to the initiation of antimicrobial therapy showed no growth. The patient underwent aortic valve and root replacement and a 16S ribosomal RNA polymerase chain reaction (16S rRNA PCR) of the resected aortic valve tissue, using the additional primer set 785F/1175R targeting the V5-7 region of 16S rRNA, identified C. canimorsus. The patient was treated post-operatively with a 6-week course of meropenem and made a good recovery. DISCUSSION: Suspicion of C. canimorsus causing infective endocarditis should be considered in culture-negative infective endocarditis in individuals who have close contact with dogs or cats. Those who are immunocompetent can be susceptible to this infection and so this diagnosis should not be disregarded in healthy individuals. A 16S rRNA PCR can help identify this bacterium and should be used early in cases of culture-negative infective endocarditis.

A Case Series on Cardiac and Skeletal Involvement in Two Families with PRKAG2 Mutations.

BACKGROUND: PRKAG2 is a rare autosomal dominant syndrome that mainly presents with hypertrophic cardiomyopathy, ventricular preexcitation, and conduction abnormalities. This case report demonstrates that the PRKAG2 mutation presents with various phenotypes already in pediatric patients. CASE SUMMARY: We describe the clinical and investigative findings in two families with a PRKAG2 mutation from the different variants in the gene on chromosome 7q36.1, emphasising that the variability of phenotypes and that presentation in childhood is common. Furthermore, we highlight that skeletal myopathy and hypertrophic cardiomyopathy are significant debilitating characteristics of the PRKAG2 mutation. CONCLUSION: In our report of adult and pediatric patients, early presentation in childhood with hypertrophic cardiomyopathy and skeletal muscle involvement was common, demonstrating the challenges of the clinical management of PRKAG2 mutations.

Lipoprotein(a) in patients with aortic stenosis: Insights from cardiovascular magnetic resonance.

BACKGROUND: Aortic stenosis is the most common age-related valvular pathology. Patients with aortic stenosis and myocardial fibrosis have worse outcome but the underlying mechanism is unclear. Lipoprotein(a) is associated with adverse cardiovascular risk and is elevated in patients with aortic stenosis. Although mechanistic pathways could link Lipoprotein(a) with myocardial fibrosis, whether the two are related has not been previously explored. In this study, we investigated whether elevated Lipoprotein(a) was associated with the presence of myocardial replacement fibrosis. METHODS: A total of 110 patients with mild, moderate and severe aortic stenosis were assessed by late gadolinium enhancement (LGE) cardiovascular magnetic resonance to identify fibrosis. Mann Whitney U tests were used to assess for evidence of an association between Lp(a) and the presence or absence of myocardial fibrosis and aortic stenosis severity and compared to controls. Univariable and multivariable linear regression analysis were undertaken to identify possible predictors of Lp(a). RESULTS: Thirty-six patients (32.7%) had no LGE enhancement, 38 (34.6%) had midwall enhancement suggestive of midwall fibrosis and 36 (32.7%) patients had subendocardial myocardial fibrosis, typical of infarction. The aortic stenosis patients had higher Lp(a) values than controls, however, there was no significant difference between the Lp(a) level in mild, moderate or severe aortic stenosis. No association was observed between midwall or infarction pattern fibrosis and Lipoprotein(a), in the mild/moderate stenosis (p = 0.91) or severe stenosis patients (p = 0.42). CONCLUSION: There is no evidence to suggest that higher Lipoprotein(a) leads to increased myocardial midwall or infarction pattern fibrosis in patients with aortic stenosis.