The incidence of significant pericardial effusion and tamponade following major aortic root surgery.

OBJECTIVE: To examine the hypothesis that the incidence of significant pericardial effusion following aortic root surgery is higher than anticipated after cardiac surgery. DESIGN: A retrospective data analysis. SETTING: A tertiary referral centre for cardiothoracic surgery. SUBJECTS: All patients undergoing aortic root surgery either with or without aortic valve replacement between January 1991 and July 1993. RESULTS: Three patients developed late cardiac tamponade (7-10 days post-operatively) and a further three developed clinically significant pericardial effusions as a result of post-pericardiotomy syndrome. The 31.6% (95% confidence limit: 12.5-56%) incidence of significant pericardial effusions following aortic root surgery is therefore significantly higher than anticipated after cardiac surgery (0.8-6). CONCLUSION: These data support the hypothesis that the incidence of significant pericardial effusion following aortic root surgery is higher than anticipated after cardiac surgery. We recommend that echocardiography is routinely performed during the post-operative period in these patients to exclude significant pericardial effusions.

Does ischemic preconditioning in the human involve protein kinase C and the ATP-dependent K+ channel? Studies of contractile function after simulated ischemia in an atrial in vitro model.

Protein kinase C (PKC) and the ATP-dependent K+ channel (KATP channel) have been implicated in the mechanism of ischemic preconditioning in animal models. This study investigated the role of KATP channels and PKC in preconditioning in human myocardium and whether KATP channels are activated via a PKC-dependent pathway. Right atrial trabeculae were superfused with Tyrode's solution and paced at 1 Hz. After stabilization, muscles underwent one of nine different protocols, followed by simulated ischemia (SI) consisting of 90 minutes of hypoxic substrate-free superfusion paced at 3 Hz and then by 120 minutes of reperfusion. Preconditioning consisted of 3 minutes of SI and 7 minutes of reperfusion. The experimental end point was recovery of contractile function after SI, presented here as percentage recovery (%Rec) of baseline function. %Rec was significantly improved by preconditioning by the KATP channel opener cromakalim (CK), and by the PKC activator 1,2-dioctanoyl-sn-glycerol (DOG) compared with nonpreconditioned controls when these treatments were given before the SI insult (control group, 29.5 +/- 3.6%; preconditioned group, 63.5 +/- 5.4%, CK-treated group, 52.9 +/- 3.1%; and DOG-treated group, 48.0 +/- 3.5%; P < .01). The effects of CK could be blocked by the KATP channel blocker glibenclamide (%Rec, 17.8 +/- 3.5%). Preconditioning could be blocked by the PKC antagonist chelerythrine (%Rec, 24.1 +/- 5.0%) and the KATP blocker glibenclamide (%Rec, 24.8 +/- 3.1%). The effects of DOG could also be blocked by glibenclamide (%Rec, 23.1 +/- 2.3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Osteomyelitis and infective endocarditis.

Osteomyelitis is thought to occur as a complication of infectious endocarditis in as many as 6% of cases of endocarditis. We describe this association in three patients. Osteomyelitis may be difficult to diagnose in patients with endocarditis because symptoms such as fever, bone pain and stiffness are common to both illnesses, therefore physicians need to have a high index of suspicion to avoid missing this important complication. We recommend that patients with endocarditis and persistent or localized musculoskeletal symptoms should be investigated to exclude osteomyelitis. Plain radiographs can be normal in 50% of cases of osteomyelitis in the early stages or show only minor abnormalities, but bone scans are highly sensitive. We suggest that a bone scan is performed if radiography is unhelpful, since a diagnosis of osteomyelitis can effectively be excluded if the bone scan is normal. We advocate close follow-up of these patients with prolonged antibiotic treatment consisting of at least 6 weeks of intravenous therapy, and 3 months or longer of oral therapy.

Protein kinase C. Its role in ischemic preconditioning in the rat.

The present study investigated whether protein kinase C (PKC) plays a role in ischemic preconditioning in the rat heart. Chelerythrine, a specific antagonist of PKC, and 1,2-dioctanoyl-sn-glycerol (DOG), a diacylglycerol analogue and specific antagonist of PKC, were used to determine whether preconditioning could be blocked or triggered, respectively. Sprague-Dawley rats were anesthetized and instrumented for coronary occlusion and reperfusion. All animals were subjected to 45 minutes of regional ischemia (ISC) followed by 2.5 hours of reperfusion. The preconditioning protocol consisted of 5 minutes of ischemia and then 10 minutes of reperfusion. There were six groups: (1) control (group C, n = 5), (2) preconditioned and ISC (group PC, n = 6), (3) chelerythrine given 2 minutes before ISC (group CC, n = 5), (4) preconditioned and chelerythrine given 2 minutes before ISC (group PCC, n = 6), (5) DOG (dissolved in dimethylsulfoxide [DMSO]) given 10 minutes before ISC (group CD, n = 5), and (6) DMSO given 10 minutes before ISC (group DMSO, n = 3). The end point was infarct size measured using triphenyl tetrazolium chloride and expressed as a percentage of the volume at risk (I/R), measured with fluorescent particles. I/R was significantly reduced by preconditioning (group C, 58.6 +/- 5.0%; group PC, 32.7 +/- 6.3%; P < .01) and by the PKC agonist DOG, which reduced I/R to a similar extent as preconditioning (group C, 58.6 +/- 5.0%; group CD, 28.0 +/- 7.0%; P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Ischaemic preconditioning protects hypertrophied myocardium.

OBJECTIVE: Clinical and experimental evidence suggests that hypertrophied myocardium is more susceptible to injury from ischaemia than normal myocardium. This study was designed to investigate whether preconditioning confers protection on hearts with moderate hypertrophy. METHODS: Cardiac hypertrophy induced by hypertension was produced in rats by giving saline drinking fluid and subcutaneous deoxycorticosterone acetate for four weeks. After thoracotomy, localisation of the left main coronary artery and stabilisation, groups of hypertensive animals with cardiac hypertrophy (HT) and their age matched normotensive controls (NT) underwent a preconditioning protocol consisting of 5 min occlusion of the left main coronary artery followed by 10 min reperfusion. This was followed by 45 min ischaemia and at least 2.5 h reperfusion. Control animals in the hypertrophied and normotensive groups were treated identically but were not subjected to the preconditioning protocol. Thus there were four experimental groups: HT preconditioned (n = 8), HT control (n = 7), NT preconditioned (n = 7), and NT control (n = 7). Infarct size was measured using triphenyl tetrazolium chloride and was expressed as a percentage of the volume at risk, measured with fluorescent particles. RESULTS: Heart weight was greater (p < 0.01) in the HT groups than in the NT groups [HT preconditioned 1.7(SEM 0.06) g, HT control 1.71(0.02) g, NT preconditioned 1.3(0.04) g, NT control 1.31(0.03) g]. Infarct to risk volume ratio (I/R) was significantly lower (p < 0.05) in the preconditioned groups as compared with controls [HT preconditioned 19.1(1.5)% v HT control 67.1(5.6)%, and NT preconditioned 33.4(5.5)% v NT control 77.1(3.8)%]. There was no significant difference in the volume at risk of infarction between the four groups. CONCLUSIONS: Ischaemic preconditioning can induce myocardial protection in hypertrophied myocardium; this is the first study to demonstrate preconditioning in hypertrophy.

Secundum atrial septal defect repair: long-term surgical outcome and the problem of late mitral regurgitation.

This study examines the clinical and surgical outcome of a group of 55 patients (mean age 33 years) with secundum atrial septal defect who underwent surgical repair of this defect between 1981 and 1990. A group of 25 of these patients underwent late echocardiographic follow-up. Fifty-two patients underwent repair by direct suturing and three by patch closure. Surgical mortality was nil. There was one late death of a 58 year old who died from cardiac failure 4 years after surgery. Late postoperative morbidity consisted of two patients; one, age 63 at the time of surgery, required mitral and tricuspid valve replacement 6 years later and one, age 77 at surgery, developed cardiac failure 3 years later. Atrial fibrillation persisted in the six patients who had the rhythm before surgery and developed postoperatively in two patients aged 54 and 58. Two patients aged 49 and 57 developed immediate postoperative sinus node dysfunction requiring permanent pacing. The mean age at surgery of those six patients who suffered cardiac morbidity was 60 years. The patients with preoperative angiographic evidence of mitral valve prolapse were significantly older (P < 0.001) and had higher mean pulmonary artery pressures (P < 0.001) than patients with normal valves. There was no significant relationship between shunt size and mitral valve prolapse. Echocardiographic follow-up showed persistent mitral valve prolapse in all nine patients who developed the condition preoperatively. Five patients developed mitral valve prolapse with mitral regurgitation postoperatively, one of whom needed subsequent mitral and tricuspid valve replacement. These five patient were on average older (mean age 54) but the group was too small to prove significance. The follow-up data illustrate the current low mortality and morbidity associated with surgical closure of atrial septal defects. Late postoperative echocardiography had revealed not only that mitral valve prolapse persists in those patients who developed the condition pre-operatively but that new cases of mitral valve prolapse with mitral regurgitation can occur after atrial septal defect closure.

Congenital left ventricular diverticula: a rare cause of sudden cardiac death.

Congenital left ventricular diverticula are a rare cause of sudden cardiac death. We describe the first reported case of ventricular fibrillation in association with congenital diverticula of the heart. The diagnosis of left ventricular diverticula was made by cardiac catheterization and confirmed by magnetic resonance imaging. Treatment was initiated with anti-arrhythmic and anticoagulant drugs to prevent life-threatening arrhythmias and emboli.

Endocarditis due to Salmonella Dublinae.

We describe, to the best of our knowledge, the first reported case of endocarditis due to Salmonella Dublinae, which occurred in a patient with surgically corrected congenital heart disease. The diagnosis was established from positive blood cultures and echocardiography, and the patient was treated by intravenous antibiotic therapy with clinical success at six months follow up. The diagnosis and its implications for management are discussed, together with a review of previously reported cases of endocarditis caused by the Salmonella group of organisms.

Impending paradoxical embolism: a rare but important diagnosis.

A man aged 50 presented with a history of a cerebrovascular accident and arterial embolism at two discrete peripheral sites. Echocardiography showed thrombus trapped in an interatrial site and impending paradoxical embolism was diagnosed. Treatment with heparin was started and the potentially embolic intracardiac material was removed at open heart surgery. The patient was treated with warfarin and made a good recovery. This is only the third case report of impending paradoxical embolism diagnosed in life.