Herz
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Infection of an intracardiac prosthesis, the incidence of which is about 2.5% among patients having undergone valve replacement, is a serious complication with considerable morbidity and mortality. Early prosthetic valve endocarditis (PVE), with an onset within 60 days of valve replacement, accounts for approximately one-third of all cases, while the remaining two-thirds, occur more than two months postoperatively (late prosthetic valve endocarditis). Prosthetic valve endocarditis is most commonly caused by Staphylococcus epidermidis, less frequently by viridans streptococci, Staphylococcus aureus, and gram-negative bacilli. ⋯ Over the last ten years the overall mortality of prosthetic valve endocarditis was 53.8%; 73.6% in early and 43% in late prosthetic valve endocarditis. More recently, however, the survival rate appears to be improving. In general, the mortality associated with prosthetic valve endocarditis caused by fungi and Staphylococcus aureus is highest and that of streptococci lowest.(ABSTRACT TRUNCATED AT 400 WORDS)
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Since the introduction of effective antimicrobial therapy, the leading cause of death in patients with infective endocarditis is no longer sepsis but, rather, congestive heart failure. The mortality is higher in patients with severe heart failure due to infective endocarditis who are treated with medical therapy only than in those who additionally undergo cardiac valve replacement. The mortality is also higher in patients with severe heart failure due to aortic infective endocarditis (40 to 93%) than in those with heart failure due to mitral infective endocarditis (17 to 66%). ⋯ Although, in at least 70% of patients, blood cultures may be rendered sterile within one week of initiation of appropriate antimicrobial therapy, patients with infective endocarditis due to staphylococci, multiply-resistant gram-negative bacilli, fungi, Q-fever or those with myocardial abscess or multiple relapses may require surgical intervention. While the overall incidence of clinically apparent emboli has been reported to be as high as 30%, in a ten-year observation period at the Mayo Clinic, the rate was 5.6%. Patients with echocardiographic evidence of large or mobile vegetations and those with infective endocarditis cause by microorganisms associated with a high risk of embolization such as slow-growing fastidious gram-negative bacilli, fungi (especially Aspergillus) and nutritionally-variant viridans streptococci should be considered candidates for surgery irrespective of a history of emboli.(ABSTRACT TRUNCATED AT 400 WORDS)
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Exercise tests were performed on 50 patients with hypertrophic obstructive cardiomyopathy (HOCM) and 19 patients with hypertrophic nonobstructive cardiomyopathy (HNCM) of NYHA classes I to IV, and on 16 patients with congestive cardiomyopathy (CCM) of NYHA classes III and IV as well as, for detection of latent cardiomyopathy (LCM), i.e. functional impairment during exercise with normal findings at rest, on 102 patients with typical or atypical angina pectoris and ECG abnormalities of unknown etiology (left bundle branch block or ST segment depression) but normal coronary arteries and normal left and right ventriculogram. Measurements included heart rate, stroke volume, cardiac output, pulmonary artery pressure and minimal cardiac transit times of Indium-113m. ⋯ The findings suggest that 1. the functional classification based on the patients' complaints often differs from the grade of hemodynamic impairment detected by exercise testing, 2. therapeutic effects (propranolol or surgery in HOCM, prazosin in CCM) are more pronounced under exercise as compared with resting conditions. Latent cardiomyopathy can be diagnosed only by detection of impaired function during exercise (increased pulmonary artery pressure, impaired myocardial lactate extraction during high-rate stimulation), since ventricular function and hemodynamics are normal at rest.
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Factors affecting the contraction of isolated cardiac muscle, preload, afterload and contractility, in addition to the heart rate, are also the primary determinants of the cardiac output in the intact ventricle. In the intact heart, ventricular end-diastolic wall stress is analogous to the preload and within physiologic limits ultimately determines the resting length of the sarcomeres in the ventricular wall. The relationship between the end-diastolic pressure and the stroke volume can be used to describe ventricular function and the relationship between stroke volume and end-diastolic volume represents the ejection fraction. ⋯ Construction of a line connecting points of end-systolic pressure-volume values corresponds with that of the force-velocity relationship, the slope of which may accurately reflect the ventricular contractility. None of these indexes, however, completely represents the force-velocity-length relationship of the intact heart. At present, the best measurements of contractility combine use of various parameters as well as data obtained from a series of contractions.