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Vol. 7, No. 5
May 2002


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LITERATURE MONITOR:
A R
EVIEW OF RECENTLY PUBLISHED CLINICAL ARTICLES

HEART FAILURE RATES INCREASE DURING WINTER

The incidence of myocardial infarction (MI) and sudden death increases during the winter months. The reason for this may be the body’s physiologic reaction to cold temperatures coupled with an increased incidence of seasonal respiratory infections, especially influenza. Stewart et al decided to study these factors in relation to higher rates of hospitalization for and death from heart failure (HF).

Researchers used the Scottish Morbidity Record to track all hospital discharges with a diagnosis of congestive HF or left HF/acute pulmonary edema for each calendar month between 1990 and 1996. The number of HF deaths in this same population was identified from 1990 to 1997.

The investigators found that the number and rate of hospitalizations for HF was markedly higher in the winter than summer. In both men and women, the greatest seasonal variation in hospitalization occurred in those 75 years or older. The number of concomitant diagnoses of respiratory disease or acute MI also increased during the winter.

A strong seasonal variation in mortality was also noted (Figure 1). The number of men who died in the Decembers between 1990 and 1997 was 16% greater than average; in women, the number of deaths in December was 21% greater than average. The poorer long-term survival in winter suggests that those with more severe HF may be prone to winter exacerbations.

In light of these observations, Stewart et al strongly recommend increased vigilance of patients with HF during the winter months and immunization with pneumococcal and influenza vaccines.

Stewart S, McIntyre K, Capewell S, McMurray JJV. Heart failure in a cold climate: seasonal variation in heart failure–related morbidity and mortality. J Am Coll Cardiol. 2002;39:760-766.

Figure 1

Seasonal Variations on Deaths
From Heart Failure

Adapted from Stewart et al. J Am Coll Cardiol. 2002.

MECHANICAL VENTILATION REDUCES DIAPHRAGM INJURY

Mechanical ventilation (MV) may protect the diaphragm from damage during sepsis. A study of endotoxin’s effects on rats has demonstrated that MV maintains sarcolemmal integrity and improves diaphragm force production during endotoxemia.

Ebihara et al placed pathogen-free adult male Sprague-Dawley rats into three groups: a control group comprising spontaneously breathing animals, a spontaneously breathing group in which Escherichia coli lipopolysaccharide (LPS) injection was used to induce endotoxemia, and a group receiving both LPS and MV.

The researchers later excised the rats’ diaphragms and examined cell integrity using a low-molecular-weight tracer dye that could not penetrate the cytoplasm of myofibers with intact sarcolemma. The control animals showed no sign of dye uptake. In contrast, the spontaneously breathing LPS group showed cytoplasmic staining of varying degrees; the extent of this staining was significantly reduced in the LPS plus MV group.

Levels of nitric oxide and protein carbonyls, both markers of oxidative stress, were markedly higher in the two LPS groups than in the controls. This indicated that MV’s protective effects were not related to inhibition of oxidation. Investigators speculated that MV may have reduced diaphragm blood flow during endotoxemic shock or lowered the mechanical load placed on endotoxemia-weakened sarcolemma.

Ebihara S, Hussain SNA, Danialou G, et al. Mechanical ventilation protects against diaphragm injury in sepsis. Am J Respir Crit Care Med. 2002;165:221-228.

LANGERHANS’-CELL HISTIOCYTOSIS ASSOCIATED WITH POOR OUTCOMES

Survival is markedly decreased in patients with pulmonary Langerhans’-cell histiocytosis, and death often results from respiratory failure. Patients with this rare disorder also face an increased risk of hematologic malignancies, a new study has shown.

Vassallo et al evaluated the records of 102 adults (40 men, 62 women) with histopathologically confirmed pulmonary Langerhans’-cell histiocytosis. These patients ranged in age from 18 to 70 years.

During a median four years’ follow-up, there were 33 deaths, 15 of which were due to respiratory failure. The researchers estimated that median survival after diagnosis was 12.5 years, significantly shorter than that expected for healthy individuals of the same age and sex.

Sixteen noncutaneous neoplasms were diagnosed in 14 patients, all of whom were current or former smokers at the time of cancer diagnosis. Six patients had hematologic cancers.

Pulmonary Langerhans’-cell histiocytosis was also shown to significantly impair patients’ health. In comparison with the general population, these patients experienced decreased physical functioning, vitality, ability to perform role-related activities, and overall well-being. They also had markedly lower forced expiratory volume and carbon monoxide diffusing capacity.

Vassallo R, Ryu JH, Schroeder DR, et al. Clinical outcomes of pulmonary Langerhans’-cell histiocytosis in adults. N Engl J Med. 2002;346:484-490.

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