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Aims: To show reversed remodelling of the left ventricle and left atrium after upgrading to biventricular pacing in a patient with worsening heart failure due to VVIR pacing. To review the literature concerning reversed remodelling after upgrading to biventricular pacing., Methods and Results: In a 61-year-old man, with cardiomyopathy and worsening heart failure and mitral insufficiency following conventional pacing after His-bundle ablation, upgrading to biventricular pacing showed left sided reversed remodelling of the heart with decrease in mitral regurgitation in 6 months. The literature is reviewed by a Medline search between 1966-2001., Conclusion: The occasionally observed progressive heart failure after right ventricular pacing following His-bundle ablation can be reversed by upgrading to VVIR biventricular pacing and under these circumstances upgrading should be considered.

In the past 35 years many experimental studies have been performed to investigate the revascularization potential of transmyocardial revascularization and the possible working mechanisms underlying the observed clinical improvement in angina pectoris after this treatment. In this review of the experimental literature, the various methods that have been used to create transmyocardial channels and the most supported hypotheses on the working mechanism (channel patency, angiogenesis and myocardial denervation) are discussed and evaluated.

The main cardiovascular effect of aging is a rise of the systolic blood pressure due to reduced impedance of the central arteries. The resulting increase of the afterload leads to hypertrophy, increased rigidity and lengthening of the relaxation period in the left ventricle. The manifestations of ischaemia or arrhythmias are often atypical at more advanced ages and may delay diagnosis. Ejection murmur due to stenosis of the aortic valve, to calcification or degeneration, may be difficult to distinguish from a functional murmur. The cause of heart failure is usually coronary sclerosis and, less often, hypertension or a valvular defect. Systolic heart failure is associated with decreased contractility of the left ventricle and compensatory dilation, diastolic heart failure with reduced filling of the ventricles. Both forms respond well to acute treatment with antihypertensive, diuretic and (or) vasodilator drugs; the treatment in isolated diastolic heart failure should also focus on lowering the increased blood pressure and reducing the heart rate to increase the filling phase.

In cardiac surgery, recognition of peroperative myocardial infarction may improve patient selection for prolonged circulatory support. The value of enzyme histochemistry to discriminate between reversible and irreversible myocardial damage at short periods of reperfusion was studied in an in vivo model of regional ischaemia in pig hearts. The left anterior descending coronary artery (LADCA) was clamped for 45 min followed by 2 h reperfusion (group 1, n = 3). Post-mortem heart tissue showed markedly decreased activities of lactate dehydrogenase (LDH) and beta-hydroxybutyrate dehydrogenase (BDH) as demonstrated in cryostat sections, accompanied by massive leakage of LDH in the venous effluent. The depleted areas showed irreversible cell damage based on the presence of flocculent densities in mitochondria. In group 2 (n = 6), LADCA flow was reduced to 40 per cent of the base-line value followed by 2 h reperfusion. Heart tissue showed normal LDH and BDH activities, except for some cells surrounding blood vessels, which activity was minimally decreased. Flocculent densities in mitochondria were never observed. We conclude that enzyme histochemistry of LDH and BDH activity on cryostat sections is a useful tool for detecting irreversible myocardial cell damage as early as 2 h reperfusion after ischaemia of the pig heart. The technique has potential applications in the detection of peroperative infarction in human biopsies.

Controversy exists as to whether hibernating myocardium is ischemic (with evidence of lactate production and ATP breakdown) during sustained coronary hypoperfusion or whether the oxygen supply is balanced by the oxygen requirements of contractile function. To investigate the mechanical and metabolic response to a moderate reduction in regional coronary blood flow, selective coronary perfusion was performed by a carotid-coronary shunt using a small roller pump circuit in six pigs. Flow was reduced for 45 minutes to 40% of base line followed by 2 hours reperfusion at normal blood flow. No hemodynamic changes occurred during flow reduction and reperfusion. Reduction of coronary blood flow to 40% resulted in a reduction in wall motion to 40.8 +/- 6.1% of base line. Two hours of reperfusion resulted in myocardial stunning shown by persistence of wall motion abnormalities (reduction to 64.6 +/- 6.0% of base line) without histologic and electron microscopic evidence of necrosis. The metabolic response to hypoperfusion varied from nil to substantial, measured as nucleotide catabolism and lactate production. We found no correlation between the base line normoxic contractile state and the magnitude of ischemic metabolite efflux. The efflux of lactate, inosine and uridine did not correlate with wall motion at each time during coronary flow reduction. Initial contractile recovery correlated with maximal lactate and uridine efflux during hypoperfusion. The results provide evidence that, in the in-vivo porcine myocardium, moderate coronary hypoperfusion can exist without metabolic evidence of ischemia.

A case of a 40-year old marine with bilateral optic neuritis and a branch retinal artery occlusion after vaccination is presented. Blood investigations showed no abnormalities. Cerebrospinal fluid studies revealed a lymphocytic pleocytosis and IgG antibodies against hepatitis A and rabies. Computerized tomography and magnetic resonance imaging of the brain were negative. A diagnosis of vaccine-induced auto-immune demyelinative optic neuritis was made. The clinical picture improved after systemic corticosteroid treatment.

Chest wall defects resulting from oncological operations often require prosthetic repair. The objectives of prosthetic repair are to provide a cosmetically acceptable substitute, prevent paradoxical chest wall movement, and protect vital organs. Of the many materials that have been used in these repairs, none have proved to be ideal. The aim of our study was to investigate the application of a biodegradable material--processed sheep dermal collagen--as a chest wall prosthesis. A full-thickness chest wall defect of 10 x 10 cm was created in 12 dogs; 10 had repair with a processed sheep dermal collagen prosthesis and 2, the controls, with polypropylene mesh. In this study, the biomaterial fulfilled its function as a chest wall prosthesis at 24 weeks' follow-up. No respiratory problems were seen, the chest wall remained stable with minimal and decreasing respiratory paradoxical movement, and the processed sheep dermal collagen slowly degraded and was replaced by the host collagen. Processed sheep dermal collagen offers long-term advantages because it is degradable. Late complications from a nonabsorbable prosthesis, ie, infection or disintegration of the material possibly causing extrusion or fistula formation, are avoided.