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Chronic thromboembolic pulmonary hypertension (CTEPH) is an important differential diagnosis in patients with unexplained dyspnoea. CTEPH is under-recognized and carries a poor prognosis without treatment. Surgical pulmonary endarterectomy is the preferred treatment for the majority of patients. Advances in surgical and anaesthetic techniques and post-operative intensive treatment have reduced perioperative morbidity and mortality. Pulmonary endarterectomy results in major improvement of haemodynamics and clinical status and offers excellent long-term survival. It is most often a curative treatment. The surgical treatment of CTEPH in Denmark is centralized at Aarhus University Hospital. Pulmonary vasodilators and pulmonary balloon angioplasty are supplementary treatment options in this patient group.

Pulmonary hypertension (PH) is classified into five groups. It is an important cause of dyspnoea. Echocardiography is the best non-invasive method for detecting PH and should be part of the evaluation of patients with dyspnoea. If signs of PH are detected on echocardiography, a number of other examinations should be undertaken to verify the diagnosis and classify PH correctly, as the treatment depends on the subtype of PH. The prognosis of PH is poor, but early detection and treatment can improve the course for some of the patients. Surgery can often cure chronic thromboembolic pulmonary hypertension.

Mortality in untreated pulmonary embolism is high and short-term outcome depends on a timely diagnosis. In this case telemedicine involving 12-lead ECG and GSM-based communication between the patient in the ambulance and the telemedical staff resulted in remote pre-hospital suspicion of acute pulmonary embolism. The ambulance was referred directly to the nearest department of cardiology where acute CT and echocardiography confirmed the diagnosis. Acute trombolysis was successful. Telemedicine may be beneficial in other medical emergencies than acute myocardial infarction.

Blockade of endothelin receptors is a new drug principle for the treatment of pulmonary arterial hypertension. Bosentan is a competitive blocker of endothelin receptors administered by the oral route. In clinical trials it has been shown to increase the functional capacity of patients with pulmonary arterial hypertension. This article describes the background, results of clinical trials, and practical guidelines for the use of bosentan in pulmonary arterial hypertension.

Spontaneous dissection of the coronary artery is a rare cause of sudden death and myocardial infarction. We report three cases in women aged 32, 38, and 55 years. One patient was one week post partum. In one case all three coronary arteries were involved. Two patients underwent coronary artery bypass grafting and one died of acute heart failure. The epidemiology, aetiology, and clinical manifestations are briefly described. We suggest that coronary angiography should be considered in young women with acute myocardial infarction and few risk factors of atherosclerosis.

Cardiac complications occur with an incidence of 2-6% and are a main cause (15-20%) of mortality after non-cardiac surgery. Cardiac risk should be determined and reduced by treatment preoperatively and by an intraoperative and postoperative care that has been adjusted to the increased risk. This review provides recommendations concerning risk evaluation and management.

A 27-year-old woman presented during a football match with sudden cardiac arrest due to ventricular fibrillation. After electrical defibrillation the electrocardiogram showed sinus rhythm with left bundle branch block. Ventriculography, echocardiography and magnetic resonance imaging revealed an aneurysm in the basal part of the ventricular septum and another aneurysm on the anterior wall of the right ventricle. She had normal coronary arteries. Ventricular tachycardia was induced in the outflow tract of the right ventricle during electrophysiological study. She was treated surgically by aneurysmectomy and cryocoagulation. No ventricular tachyarrythmia could be provoked at postoperative electrophysiological testing. Histological examination of the right ventricular aneurysm showed the presence of noncaseating granulomas and scar tissue consistent with cardiac sarcoidosis. She had no other systemic manifestations of the disease. The patient was doing well and had no cardiac symptoms after the operation. She died suddenly of unknown cause 21 months later. No autopsy was performed.

A 72-year-old man with an AAI-rate-responsive pacemaker (Siemens-Elema Sensolog III; unipolar pacing electrode) was admitted for cardioversion of atrial fibrillation. Electrical defibrillation was followed by severe nodal bradycardia and pacemaker malfunction characterized by loss of atrial capture. The pacemaker failure was due to an acute rise in the stimulation threshold, possibly secondary to current-induced tissue damage at the electrode-endomyocardial interface. It is recommended that a pacemaker is reprogrammed to maximum pulse voltage amplitude prior to elective DC-cardioversion and that serial measurements of the myocardial stimulation threshold are performed after defibrillation. Other factors essential for the management of the pacemaker patient who requires electrical defibrillation are outlined.

A 44-year-old woman was seen on three separate occasions for acute pulmonary edema which had developed 30 minutes after ingestion of a single hydrochlorothiazide-amiloride (Moduretic) tablet. Eighteen cases of hydrochlorothiazide-induced pulmonary edema have been reported previously. Clinical findings and investigations in the present and previous cases indicate a noncardiogenic cause for the pulmonary edema. Increased pulmonary vascular permeability is probably involved. So far, attempts to demonstrate an immunological mechanism have failed and the pathophysiology remains uncertain. The reaction may be difficult to differentiate from left ventricular failure in patients with cardiac disease. Attention should be drawn to this severe but rare side effect of a frequently used diuretic.

A case of fatal fulminant hepatitis following treatment with disulphiram in a man aged 34 year is reported. Acute toxic hepatitis produced by disulphiram is a rare but serious side effect with a lethality about 40%. In the case reported here, immediate withdrawal of disulphiram administration on the earliest signs of hepatitis did not prevent toxic development of severe hepatic necrosis.