[Review of Changes in Group A Streptococcal Infections. Case reports: Streptococcal toxic shock syndrome and necrotizing fasciitis.].

In the last years there has been an increase in serious invasive group A streptococcal infections. Necrotizing fasciitis is one of them. These infections have mostly affected young and middle aged people without known risk factors. The first symptoms are usually pain and influenza like symptoms and then following rapid deterioration with shock and multiorgan failure. This has been called streptococcal toxic shock syndrome (STSS). The literature on STSS and necrotizing fasciitis is reviewed. Symptoms and signs and treatment of STSS are discussed, as are theories about increased pathogenicity of group A streptococcus and pathogenesis of STSS. Increased pathogenicity seems largely due to a combination of M types 1 or 3 and streptococcal pyrogen exotoxin (SPE) production. M proteins increase the pathogenicity and SPE can cause shock and multiorgan failure. Neutralising anti-M and anti-SPE antibodies most likely protect against STSS. Two cases are reviewed, both young men with invasive group A streptococcal infections, serotype M-l. One developed STSS and died in three days the other developed an typical abscess and responded to therapy with drainage and antibiotics.

Native-valve endocarditis due to Neisseria sicca: case report and review.

Many species of the Neisseria, gram-negative diplococci that are frequent respiratory commensals in humans, have been regarded as being nonpathogenic or as causing disease in only immunocompromised hosts; in contrast, gram-negative diplococci such as Neisseria meningitidis and Neisseria gonorrhoeae are known pathogens. We report a case in which Neisseria sicca was the cause of serious infection (with catastrophic consequences) in an immunocompetent patient and review the world literature on endocarditis due to N. sicca.

Antianginal and anti-ischemic efficacy of nicorandil compared with nifedipine in patients with angina pectoris and coronary heart disease: a double-blind, randomized, multicenter study.

Patients with stable, effort-induced angina pectoris and a typical combination of anginal pain and ischemic ST depression in exercise tolerance tests were randomized to treatment for 8 weeks with nicorandil (a newly developed antianginal and anti-ischemic drug) or nifedipine. After 4 weeks, the dosage of nicorandil was increased from 10 mg b.i.d. to 20 mg b.i.d., but the recommended dosage of nifedipine, 20 mg b.i.d., was kept constant during the study period. Double-blind treatment was preceded by a 2-week prephase during which patients were treated with isosorbide dinitrate. During the study period, patients were asked to report the rate of anginal attacks and consumption of sublingual nitroglycerin. Measurements of blood pressure and heart rate at rest and during exercise always were performed 2 h after drug intake. Fifty-eight patients were randomized--29 to nicorandil and 29 to nifedipine. There were large individual variations in anginal attack rates, which makes group comparisons difficult, but in the nicorandil group, the anginal attack rate decreased significantly compared with baseline frequency. Systolic blood pressure at rest was reduced significantly only with the highest dose of nicorandil, but nifedipine had a significant effect on both systolic and diastolic blood pressures as well as on the heart rate. Both treatments significantly increased exercise duration, time to onset of angina pectoris, and time to 1-mm ST depression. In the nicorandil group, an improvement was noted with the 20-mg dose compared with the 10-mg dose, but no significant differences were noted between the nicorandil and nifedipine groups after either 4 or 8 weeks of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Doppler echocardiographic detection of traumatic ventricular septal defect--a case report.

A case of traumatic ventricular septal defect diagnosed by Doppler echocardiography is described. The characteristic pulsed Doppler findings of a left-to-right shunt were recorded and the two-dimensional echocardiographic images of septal interruption were shown. Combined Doppler and two-dimensional echocardiography enhances the ability to detect the presence of a ventricular septal defect. Doppler echocardiography appears to be a useful noninvasive imaging modality in the evaluation of patients with cardiac trauma.

The clinical spectrum of tricuspid regurgitation detected by pulsed Doppler echocardiography.

The clinical diagnosis of tricuspid regurgitation (TR) is often difficult. Two-dimensional pulsed Doppler echocardiography offers a sensitive and specific method for detecting and semi-quantitating tricuspid regurgitation. The clinical, radiographic, radionuclide, echocardiographic, and when available, the right cardiac catheterization findings were evaluated in 36 patients with a diagnosis of tricuspid regurgitation by pulsed Doppler. Ten healthy subjects served as controls. The underlying cardiac cause was rheumatic heart disease in 7 (20%), ischemic heart disease in 12 (33%), dilated cardiomyopathy in 5 (14%), hypertensive heart disease in 2 (5%), aortic valve stenosis and/or regurgitation in 3 (8%), mitral valve prolapse with mitral regurgitation in 1 (3%), and congenital heart disease in 6 (17%). Seven patients (19%) had a temporary or permanent transvenous right ventricular pacing wire. A systolic murmur was heard in 29 patients (81%) with 16 (46%) having an elevated jugular venous pressure. Tricuspid regurgitation was clinically suspected in only 2 patients (6%). Isolated tricuspid regurgitation was uncommon, seen in 6 patients (17%), and usually secondary to congenital heart disease, ischemic heart disease, with the use of a transvenous pacing wire and following mitral valve replacement. Right cardiac catheterization was performed in 10 patients, of which 7 demonstrated elevated right atrial and pulmonary artery pressure. Pulsed Doppler echocardiography offers a practical and accurate method of detecting and evaluating the severity of tricuspid regurgitation. Tricuspid regurgitation is generally a functional disorder, and frequently occurs in association with left sided valvular heart disease, cardiomyopathy or congenital heart disease.