Periodontal bacteria DNA findings in human cardiac tissue - Is there a link of periodontitis to heart valve disease?

BACKGROUND: The aim of the study was to detect periodontal pathogens DNA in atrial and myocardial tissue, and to investigate periodontal status and their connection to cardiac tissue inflammation. METHODS: In 30 patients, biopsy samples were taken from the atrium (A) and the ventricle myocardium (M) during aortic valve surgery. The dental examination included the dental and periodontal status (PS) and a collection of a microbiological sample. The detection of 11 periodontal pathogens DNA in oral and heart samples was carried out using PCR. The heart samples were prepared for detecting the LPS-binding protein (LBP), and for inflammation scoring on immunohistochemistry (IHC), comprising macrophages (CD68), LPS-binding protein receptor (CD14), and LBP (big42). RESULTS: 28 (93%) patients showed moderate to severe periodontitis. The periodontal pathogens in the oral samples of all patients revealed a similar distribution (3-93%). To a lesser extent and with a different distribution, these bacteria DNA were also detected in atrium and myocardium (3-27%). The LBP was detected in higher amount in atrium (0.22±0.16) versus myocardium (0.13±0.13, p=0.001). IHC showed a higher inflammation score in atrial than myocardial tissue as well as for CD14, CD68 and for LBP. Additional, periodontal findings showed a significant correlation to CD14 and CD68. CONCLUSION: The results provide evidence of the occurrence of oral bacteria DNA at the cardiac tissue, with a different impact on atrial and myocardial tissue inflammation. Influence of periodontal findings was identified, but their relevance is not yet distinct. Therefore further clinical investigations with long term implication are warranted.

Histological changes in neonatal kidneys after cardiopulmonary bypass and deep hypothermic circulatory arrest.

BACKGROUND: Renal failure after open-heart surgery is a serious complication resulting in increased mortality and morbidity. The aim of the study was to find out whether different strategies for open-heart surgery would result in renal histological differences in a neonatal animal model. METHODS: The renal tissue of newborn piglets was examined after mild hypothermic cardiopulmonary bypass (CPB group; n = 10), deep hypothermic circulatory arrest (DHCA group; n = 8), instrumentation without extracorporeal circulation (sham; n = 3), and the data were compared with those of normal porcine neonatal kidneys (control; n = 6). The severity of tissue damage was graded using a 4-point scoring system (0: normal morphology, 3: severe damage). Apoptotic cells and granulocytes were counted. RESULTS: The histological score was higher in all groups compared with controls ( P < 0.05) and higher in the CPB group compared with the DHCA group ( P < 0.05). More apoptotic cells and granulocytes were found in the CPB group compared with controls and the DHCA group ( P < 0.05). CONCLUSIONS: Although changes in the kidney tissue of newborn piglets are detectable after any cardiac procedure, changes are more profound after cardiopulmonary bypass with mild hypothermia.

Chronic heart failure induced by multiple sequential coronary microembolization in sheep.

OBJECTIVE: Although a large variety of animal models for acute ischemia and acute heart failure exist, valuable models for studies on the effect of ventricular assist devices in chronic heart failure are scarce. We aimed to establish a stable and reproducible animal model of chronic heart failure in sheep. METHODS: Sheep (n=8, 77 +/- 4 kg) were anesthesized and a 5F sheath was implanted into the left carotid artery. The left main coronary artery was catheterized under flouroscopic guidance and bolus injection of polysterol microspheres (90 microm, n=25.000) was performed. Microembolization (ME) was repeated up to three times in two to three week intervals until animals started to develop stable clinical signs of heart failure. Clinical and echocardiographic data were analyzed at baseline (base) and at three months (3 mo) after first ME. All animals were followed for 3 months after first microembolization and then sacrificed for histological examination. Another four healthy sheep (79+/-6 kg) served as control animals. RESULTS: All animals developed clinical signs of heart failure as indicated by increased heart rate at rest (68+/-4 bpm (base) to 93 +/- 5 bpm (3 mo) (p<0.05)), increased respiratory rate at rest (28+/-5 (base) to 38 +/- 7 (3 mo) (p<0.05)) and increased body weight 77 +/- 2 kg to 81 +/- 2 kg (p<0.05) due to pleural effusion, peripheral edema and ascites. Echocardiographic evaluation revealed significantly an increase of left ventricular enddiastolic diameter from 46 +/- 3 mm (base) to 61 +/- 4 mm (3 mo) (p<0.05). Clinically and echocardiographically no significant changes were revealed in healthy control animals. CONCLUSIONS: We conclude that multiple sequential intracoronary microembolization can effectively induce myocardial dysfunction with clinical and echocardiographical signs of chronic ischemic cardiomyopathy. The present model may be suitable in experimental work on heart failure and left ventricular assist devices, e.g. for studying the impact of mechanical unloading, mechanisms of recovery and reverse remodeling.