[Congestive heart failure--etiology and diagnostic procedures]. / Kronisk hjertesvikt--etiologi og diagnostikk.

Congestive heart failure is a major health problem in the western world and the prevalence of patients with this diagnosis increases. About 2% of the adult population are affected; the majority are elderly, which represents a challenge when it comes to assessment and treatment. This article concerns the aetiology and diagnosis of congestive heart failure and provides a suggestion for guidelines. The proposed guidelines are aimed at primary, secondary and third line health care providers in Norway, and are based on previously published Norwegian guidelines and international guidelines. Hypertension and coronary artery disease account for 75-80% of known cases of congestive heart failure. The patient's history and risk factors must be investigated. Laboratory tests emphasising organ functions are important, and these should include measurement of B-type natriuretic peptide (BNP). Electrocardiograms and chest X-rays should be taken as well. All patients with suspected impaired left ventricular ejection fraction should undergo an echocardiographic examination. Invasive tests, and non-invasive imaging should be used for selected groups of patients only.

[Treatment of congestive heart failure]. / Behandling av kronisk hjertesvikt.

The Working Group on Heart Failure of the Norwegian Society of Cardiology here presents a revised programme for the treatment of congestive heart failure. Possible surgical and percutaneous interventions should be considered, and non- pharmacological measures taken as indicated for each patient. ACE-inhibitors are the first-line pharmacological therapy in heart failure with reduced left ventricular ejection fraction (< 40%). Possible adverse effects on blood pressure, renal function and electrolytes necessitate close monitoring of these variables. Beta-blockers should be considered in patients with symptomatic heart failure. If ACE-inhibitors are not tolerated, an angiotensin- II-blocker can be the added. Diuretics should only be used as adjunctive therapy to ACE-inhibitors. Aldosterone antagonists have a proven effect on survival, but close monitoring of potassium levels is imperative. Especially in the elderly, the renal function and level of electrolytes must be monitored closely. Device therapy, such ac cardiac resynchronization therapy and implantable cardioverter defibrillators, are only indicated for selected patients. ACE-inhibitors, diuretics and beta-blockers are the drugs-of-choice for patients with congestive heart failure with preserved systolic function. Health care for patients with congestive heart failure must be well organized on different levels of care and with multidisciplinary teams involved. The goal is to reduce morbidity and mortality in the heart failure population. This programme is meant for primary, secondary and third line health care providers in Norway.

[Use of nuclear cardiologic methods]. / Bruk av nukleaerkardiologiske metoder.

A review of nuclear cardiology is presented with a focus on myocardial scintigraphy, radionuclide ventriculography and positron emission tomography. Aspects of practical importance for the clinical cardiologist and general practitioner are discussed.

Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia?

It has been postulated that unsuccessful resuscitation of victims of accidental hypothermia is caused by insufficient tissue oxygenation. The aim of this study was to test whether inadequate O2 supply and/or malfunctioning O2 extraction occur during rewarming from deep/profound hypothermia of different duration. Three groups of rats (n = 7 each) were used: group 1 served as normothermic control for 5 h; groups 2 and 3 were core cooled to 15 degrees C, kept at 15 degrees C for 1 and 5 h, respectively, and then rewarmed. In both hypothermic groups, cardiac output (CO) decreased spontaneously by > 50% in response to cooling. O2 consumption fell to less than one-third during cooling but recovered completely in both groups during rewarming. During hypothermia, circulating blood volume in both groups was reduced to approximately one-third of baseline, indicating that some vascular beds were critically perfused during hypothermia. CO recovered completely in animals rewarmed after 1 h (group 2) but recovered to only 60% in those rewarmed after 5 h (group 3), whereas blood volume increased to approximately three-fourths of baseline in both groups. Metabolic acidosis was observed only after 5 h of hypothermia (15 degrees C). A significant increase in myocardial tissue heat shock protein 70 after rewarming in group 3, but not in group 2, indicates an association with the duration of hypothermia. Thus mechanisms facilitating O2 extraction function well during deep/profound hypothermia, and, despite low CO, O2 supply was not a limiting factor for survival in the present experiments.

Influence of substrate supply on cardiac efficiency, as measured by pressure-volume analysis in ex vivo mouse hearts.

In the present study, we tested the reliability of measurements of pressure-volume area (PVA) and oxygen consumption (MVo(2)) in ex vivo mouse hearts, combining the use of a miniaturized conductance catheter and a fiber-optic oxygen sensor. Second, we tested whether we could reproduce the influence of increased myocardial fatty acid (FA) metabolism on cardiac efficiency in the isolated working mouse heart model, which has already been documented in large animal models. The hearts were perfused with crystalloid buffer containing 11 mM glucose and two different concentrations of FA bound to 3% BSA. The initial concentration was 0.3 +/- 0.1 mM, which was subsequently raised to 0.9 +/- 0.1 mM. End-systolic and end-diastolic pressure-volume relationships were assessed by temporarily occluding the preload line. Different steady-state PVA-MVo(2) relationships were obtained by changing the loading conditions (pre- and afterload) of the heart. There were no apparent changes in baseline cardiac performance or contractile efficiency (slope of the PVA-MVo(2) regression line) in response to the elevation of the perfusate FA concentration. However, all hearts (n = 8) showed an increase in the y-intercept of the PVA-MVo(2) regression line after elevation of the palmitate concentration, indicating an FA-induced increase in the unloaded MVo(2). Therefore, in the present model, unloaded MVo(2) is not independent of metabolic substrate. This is, to our knowledge, the first report of a PVA-MVo(2) relationship in ex vivo perfused murine hearts, using a pressure-volume catheter. The methodology can be an important tool for phenotypic assessment of the relationship among metabolism, contractile performance, and cardiac efficiency in various mouse models.