Non-traumatic and non-drug-induced rhabdomyolysis.

Rhabdomyolysis (RM), a fortunately rare disease of the striated muscle cells, is a complication of non-traumatic (congenital (glycogen storage disease, discrete mitochondrial myopathies and various muscular dystrophies) or acquired (alcoholic myopathy, systemic diseases, arterial occlusion, viral illness or bacterial sepsis)) and traumatic conditions. Additionally, RM can occur in some individuals under specific circumstances such as toxic substance use and illicit drug abuse. Lipid-lowering drugs in particular are capable of causing RM. This comprehensive review will focus on non-traumatic and non-drug-induced RM. Moreover, the pathology of RM, its clinical manifestation and biochemical effects, and finally its management will be discussed.

Idiopathic pulmonary arterial hypertension in a young patient with the Cohen syndrome.

We admitted a 16-year-old boy with the Cohen syndrome to our institution for increasing dyspnoea. Investigations revealed idiopathic pulmonary hypertension. He was commenced on bosentan and oral anticoagulation and was followed up for nearly 7 years, during which he was readmitted for dynamic measurements of pulmonary artery pressure. Despite initial improvement, the right heart pressures increased again and sildenafil was added. His final hospitalisation was due to increasing breathlessness and episodes of syncope. The addition of prostacyclin conferred no reduction in pulmonary artery pressure. The patient suffered a cardiac arrest and remained intubated for 2 weeks, during which Klebsiella pneumonia and superinfection with the H1N1 swine flu virus occurred. The patient died due to multi-organ failure, nearly 7 years after his initial diagnosis. The Cohen syndrome, its phenotype and clinical findings, and the incidence and treatment of pulmonary hypertension are discussed.

Post-resuscitation care: current therapeutic concepts.

Post-resuscitation care is coming increasingly into focus. The patient with a return in spontaneous circulation (ROSC) often presents with a post-arrest 'sepsis-like syndrome', which requires a multidisciplinary implementation of timely reperfusion, proper inotropic support and monitoring, glucose control, therapeutic hypothermia, and adequate sedation in the intensive care unit (ICU). Low tidal volume (6 ml/kg) ventilation is preferred, and the standard vasopressor treatment of dobutamine, dopamine, and norepinephrine can be used to improve the patient's haemodynamic profile. Coronary revascularization should be attempted where there is evidence of ST-segment elevation myocardial infarction (STEMI), even in comatose patients. The recently published TROICA trial did not prove that thrombolysis improved survival. Glycaemic management can help decrease the length and cost of ICU stay, although the argument for tight glucose control has been recently challenged. Therapeutic hypothermia should be aggressively implemented in comatose adult patients after arrest from a shockable rhythm. Seizures are associated with a worse neurological outcome and early anti-convulsant prevention is advocated. Raised biomarkers such as NSE and S-100 beta may correlate with neurological outcome, but also overestimate the extent of cerebral damage in resuscitated patients and have a wide confidence interval. Simple neurological examination manoeuvers strongly predict death or poor outcome.

Primary stenting of an unprotected left main coronary artery total occlusion in a patient with acute myocardial infraction and cardiogenic shock.

Acute total occlusion of the left main coronary artery (LMCA) is a rare angiographic finding with very poor prognosis. We report a case of a 39-year-old man who presented with pulmonary edema and cardiogenic shock due to an acute anterior myocardial infarction. Coronary angiography, which was performed under the support of an intra-aortic balloon pump, revealed total occlusion of the LMCA. Prompt and successful percutaneous transluminal coronary angioplasty with sirolimus-stent deployment in the LMCA allowed for an uneventful recovery and discharge of the patient.

Coronary angioplasty in identical twins.

We report coronary angioplasty of the same coronary artery in identical twin sisters. The patients had similar risk factors but differed in their coronary anatomy. The angioplasties were carried out on the same day and by the same cardiologist. To our knowledge, this is the first reported follow-up of such a case.

The role of left ventricular long-axis contraction in patients with asymptomatic aortic regurgitation.

BACKGROUND: We aimed to investigate the role of long axis contraction in patients with asymptomatic chronic aorta regurgitation (AR). METHODS: In 84 consecutive patients (48 men, mean age 55.5 +/- 13.5 years) tissue Doppler imaging was performed. During catheterization, left ventricular end-diastolic pressure (LVEDP) and end-diastolic wall stress (EDWS) were calculated. RESULTS: The best predictor for group membership (exercise ejection fraction increase > or < of 5%) is the systolic wave maximal velocity (Sv) at the lateral mitral annulus (9 cm/s). Patients with Sv > 9 cm/s (45 patients) formed group I, while 39 patients with Sv < 9 cm/s formed group II. LVEDP and EDWS were higher in group II (15.5 +/- 1.9 mm Hg and 214.8 +/- 233.3 g/cm2) than in group I (10.3 +/- 1.7 mmHg and 111.8 +/- 40.8 g/cm2), P = .0001 and P = .01, respectively. CONCLUSION: In patients with asymptomatic AR, the estimation of left ventricular long axis contraction at rest, can unmask a subnormal left ventricular functional status.

Acute thrombosis of a prosthetic mitral valve.

We report the case of a patient who was transferred to our hospital with acute thrombosis of a prosthetic mitral valve. Her admission INR was subtherapeutic. The transoesophageal echocardiographic images are presented. The patient underwent urgent reoperation and made a good recovery.

Intravenous atenolol and esmolol maintain the protective effect of ischemic preconditioning in vivo.

Catecholamines bind to alpha- and beta-adrenoreceptors and are capable of preconditioning ischemic myocardium. Our purpose was to investigate the effect of acute either short or prolonged i.v. administration of beta-adrenoreceptor antagonists on ischemic preconditioning in vivo. Fifty-five anesthetized rabbits were divided into 10 groups (n=5-7 per group) and were subjected to 30-min regional ischemia of the heart after ligation of a prominent left coronary artery and 3-h reperfusion after releasing the snare. Ischemic preconditioning was obtained by three cycles of 5-min ischemia separated by 10-min reperfusion. beta-Adrenoreceptor blockade was obtained by the long acting beta-adrenoreceptor antagonist atenolol or by the short acting esmolol, which were given as a short 5-min infusion or as a prolonged 45-min infusion, starting respectively 20 min before and ending 15 min before the beginning of sustained ischemia, or starting 45 min before and ending immediately before the beginning of sustained ischemia. Atenolol was given at a rate of 0.2 mg min(-1) during 5 min or at a rate of 0.088 mg min(-1) as a 45-min infusion. Esmolol was given as an initial dose of 500 microg kg(-1) within 1 min, followed by a 4-min infusion at a rate of 50 microg kg(-1) min(-1) or as an initial dose of 3.4 mg within 1 min, followed by a 44-min infusion at a rate of 0.15 mg min(-1). Blood pressure and heart rate were continuously monitored. The infarcted and risk areas were delineated with the aid of tetrazolium chloride staining and fluorescent Zn-Cd particles. Infarct size was expressed in percent of the area at risk. All the animals without preconditioning developed an infarct size ranging between 36.3+/-2.4% and 49.6+/-7.6% (P=NS) and all the preconditioning groups developed an infarct size ranging between 14.9+/-1.2% and 21.0+/-2.2% (P=NS). All the preconditioning groups, independently of the use of beta-adrenoreceptor antagonists, had a smaller infarct size than the control group, which developed an infarct size of 47.3+/-2.5% (P<0.01). Intravenous atenolol and esmolol, independent of timing and mode of administration, does not seem to interfere with protection afforded by ischemic preconditioning in vivo.

Oral nicorandil recaptures the waned protection from preconditioning in vivo.

1. Protection from preconditioning (PC) wanes and is eventually lost when multiple bouts of short ischemia or a prolonged reperfusion interval precedes the following sustained ischemia. The activation of mitochondrial K(ATP) channels plays a pivotal role in the intracellular signaling of PC. We tested whether the K(ATP) channel opener nicorandil (nic) preserves the given protection from PC in conditions where this benefit decays and is lost. 2. Eight groups of rabbits were divided into two equal series of experiments, one without nic (placebo) and one with nic treatment. Nic was given orally for 5 consecutive days in a dose of 5 mg kg(-1) d(-1). In a second step, four additional groups were treated with nic plus the K(ATP) channel blocker 5HD and 1 additional control group with nitroglycerin only. All the animals were anesthetized and then subjected to 30 min of myocardial ischemia and 2 h of reperfusion with one of the following interventions before the sustained ischemia: Control groups to no intervention; 3PC groups to three cycles of 5-min ischemia-10-min reperfusion; 8PC groups to eight cycles of 5-min ischemia - 10-min reperfusion; and 3PC90 groups to the same interventions as the 3PC groups but with a prolonged (90 min) intervening reperfusion interval before the sustained ischemia. The infarcted and the risk areas were expressed in percent. 3. There was no significant change in infarct size between the placebo, the nic and the 5HD-nic in the control groups (41.5+/-4.7, 43.9+/-7.1 and 48.7+/-6.4%) and 3PC groups (10.3+/-3.4, 12.2+/-3.9 and 12.6+/-4.5%). However, there was a significant decrease after nic treatment in groups 8PC (47.7+/-8.8% vs 13.0+/-2.6%, P<0.01) and 3PC90 (37.3+/-6.0% vs 14.2+/-2.4%, P<0.01), which was abrogated (38.2+/-4.7 and 42.7+/-4.4%, respectively, for 8PC and 3PC90 groups). Nitroglycerin had no effect on infarct size (39.1+/-3.1%, P=NS vs other controls). 4. Oral treatment with nic recaptures the waned protection of PC, both after repetitive bouts of short ischemia or after a prolonged reperfusion interval, preserving the initially obtained benefit. Nic by itself is insufficient to initiate PC in vivo.

Doppler-derived left ventricular end-diastolic pressure prediction model using the combined analysis of mitral and pulmonary A waves in patients with coronary artery disease and preserved left ventricular systolic function.

The aim of this study was to analyze the components of mitral and pulmonary A waves and to construct a Doppler-derived left ventricular (LV) end-diastolic pressure (EDP) prediction model based on the combined analysis of transmitral and pulmonary venous flow velocity curves. Combined analysis of transmitral and pulmonary venous flow velocity curves at atrial contraction is a reliable predictor of increased LV filling pressure. The duration of pulmonary and mitral A waves is determined by the sum of respective acceleration and deceleration time. Mitral flow and left upper pulmonary vein flow velocity curves were recorded simultaneously with LVEDP in 40 consecutive patients (aged 59 +/- 8 years) with coronary artery disease and preserved LV systolic function. Differences in all parameters represent values of pulmonary minus those of mitral A wave curve. The difference in deceleration time was the strongest candidate, being included in all models. After redundancy evaluation, we reached the following model: LVEDP = 20.61 + 0.229 x difference in deceleration time (r(2) = 0.80, p <0.001). In the entire study group, the difference in duration and in deceleration time of the A wave was highly correlated with LVEDP (r = 0.79, p <0.001, and r = 0.88, p <0.001, respectively). The entire study group was further divided according to whether LVEDP was above (group I, 20 patients) or below (group II, 20 patients) the median value (15.5 mm Hg). In group I, the difference in duration and in deceleration time correlated well (r = 0.62, p = 0.01, and r = 0.75, p = 0.001, respectively) with LVEDP, whereas in group II only the difference in deceleration time correlated well (r = 0.68, p = 0.005). In patients with coronary artery disease and preserved LV systolic function, the combined analysis of mitral and pulmonary A waves can predict LVEDP. The difference in deceleration time between pulmonary and mitral A waves can reliably evaluate high and normal LVEDP.