Complete embolization of a mechanical aortic valve during trail running-a case report with a lucky ending.

Background: Complete embolization of a prosthetic heart valve is extremely rare and dangerous. This case reports a total embolization of a mechanical aortic valve and contributes to the literature regarding the diagnostic challenges related to infective endocarditis and follow-up after valvular surgery. Case summary: A 28-year-old male 11.5 years status-post a mechanical aortic valve replacement presented with acute onset of chest pain and dyspnoea while jogging. The patient lost consciousness and went into cardiopulmonary arrest with acute pulmonary oedema and circulatory shock. An echocardiogram revealed an empty aortic annulus, and a chest radiograph showed an embolized valve in the aortic arch. The patient underwent emergent removal of the embolized valve and replacement with a new mechanical aortic valve. The patient survived with minimal sequelae. At a 3-month follow-up, he had resumed work, and the only sequelae were mild left ventricular dysfunction and minor vision loss. Although he experienced no warning signs or symptoms, the most likely aetiology for embolization of the valvular prosthesis was infective endocarditis, which was revealed by re-evaluation of an echocardiogram recorded 1 month before the presentation which demonstrated a subtle motion abnormality of the valve. Conclusions: We present a case of a late complete embolization of a mechanical aortic valve most likely caused by asymptomatic infective endocarditis. The case illustrates the challenges in follow-up after valvular surgery and highlights the ultimate benefit of a well-functioning pre-hospital to hospital chain.

Acute exercise is not cardioprotective and may induce apoptotic signalling in heart surgery: a randomized controlled trial.

OBJECTIVES: During open-heart surgery, the myocardium experiences ischaemia-reperfusion injury. A single bout of moderate, 30-min exercise induces preconditioning and protects the heart from ischaemia-reperfusion injury in rats, but this has never been investigated in humans. We aimed to investigate whether 1 bout of moderate exercise 24 h prior to surgery protects against mitochondrial and cardiac damage. METHODS: Patients scheduled for elective coronary artery bypass were eligible for this pilot study. Twenty were included and randomized to the treadmill exercise group (the EX group, n = 10) 24 h preoperatively or to standard presurgical procedures (control n = 10). Right atrial (RA) and left ventricular (LV) biopsies were collected immediately before and as long as possible after aortic cross-clamping to assess the primary outcome of mitochondrial respiration by respirometry, in addition to reactive oxygen species production by fluorometry and apoptotic transcripts. Cardiac troponin T and creatine kinase myocardial brain were measured in plasma at arrival, before surgery and 6 and 24 h postoperatively. RESULTS: Mitochondrial respiration was lower in the EX group after surgery in the LV (Complex I -22%, P < 0.05 and maximal -23%, P < 0.05) and the right atrium (Complex I -25%, P < 0.05). Transcript level of the apoptosis-related marker caspase 3 was increased 1.5-fold in the LV prior to surgery in the EX group when compared with the control group, P < 0.05. Cardiac troponin T was 45% higher in the EX group than in the control group 6 h postoperatively (P = 0.03), although not significant when corrected for aortic cross-clamping time. CONCLUSIONS: Results indicate that exercise did not precondition the heart against surgery-related damage. Exercise may render the myocardium and mitochondria more vulnerable to perioperative damage. Clinical trials registration number: NCT00218985 (https://clinicaltrials.gov/ct2/show/NCT00218985).

Remote ischemic preconditioning preserves mitochondrial function and activates pro-survival protein kinase Akt in the left ventricle during cardiac surgery: a randomized trial.

BACKGROUND: Understanding the intracellular mechanisms induced by remote ischemic preconditioning (RIPC) in the human left ventricle opens new possibilities for development of pharmacological cardioprotection against ischemia and reperfusion injury. In this study we investigated the effects of RIPC on mitochondrial function, activation of pro-survival protein kinase Akt and microRNA expression in left ventricular biopsies from patients undergoing coronary artery bypass surgery (CABG). METHODS: Sixty patients were randomized to control (n=30) or RIPC (n=30). A blood pressure cuff was applied to the arm of all patients preoperatively. The cuff remained deflated in control group, whereas RIPC was performed by 3 cycles of cuff inflation to 200 mm Hg for 5 min, separated by 5 min deflation intervals. Left ventricular biopsies were obtained before and 15 min after aortic declamping. The primary outcome was mitochondrial respiration measured in situ. Secondary outcomes were activation of protein kinase Akt, assessed by western immunoblotting, and expression of microRNAs assessed by array and real-time polymerase chain reaction. RESULTS: Mitochondrial respiration was preserved during surgery in patients receiving RIPC (+0.2 µmol O2/min/g, p=0.69), and reduced by 15% in controls (-1.5 µmol O2/min/g, p=0.02). Furthermore, RIPC activated protein kinase Akt before aortic clamping (difference from control +43.3%, p=0.04), followed by increased phosphorylation of Akt substrates at reperfusion (+26.8%, p<0.01). No differences were observed in microRNA expression. CONCLUSIONS: RIPC preserves mitochondrial function and activates pro-survival protein kinase Akt in left ventricle of patients undergoing CABG. Modulation of mitochondrial function and Akt activation should be further explored as cardioprotective drug targets. CLINICAL TRIAL REGISTRATION: http://www.clinicaltrials.gov, unique identifier: NCT01308138.