Infective Endocarditis   497
though Roth spots are highly suggestive of infective endocarditis, they are also seen in patients with collagen-vascular and hematologic dis¬orders.
Other clinical manifestations may involve other organ systems as a result of thromboembolic phenomena. Rmboli to the spleen may cause left upper quadrant abdominal pain radiating to the shoulder, a splenic friction rub, or signs of a left pleural effusion. Rmboli to Ihe kidney may cause flank or back pain, suggesting renal infarction. Patients with tricuspid valve endocarditis may develop pulmonary emboli and pre¬sent with dyspnea, cough, pleuritic chest pain, and hemoptysis, espe¬cially if pulmonary infarction has occurred.
Cerebral embolism and rupture of an intracranial mycotic aneurysm are devastating complications, and the palient may present with the signs of a cerebrovascular accident; (his may distract the clinician from Ihe infectious cause of the disease. Fever and a stroke syndrome in any patient should warrant consideration of Ihe possibility of infective en¬docarditis. Most cerebral emboli involve the distribution of the middle cerebral artery or one of its branches. Clinical signs of emboli include hemiparesis. cranial nerve palsies, corticosensory loss, aphasia, ataxia, alterations in mental status, or a combination thereof. Persistent headache may be the only symptom signifying an intracranial mycotic aneurysm before rupture.

tous deposits can cause turbulence and. hence, thrombus formation. All forms of valvular disease increase the risk of endocarditis, although about 40% of elderly patients with endocarditis have either no valvular lesions or undetermined ones. Of the 60% who do have valvular dis¬ease, about 30% have rheumatic lesions, about 25% have calcified valves, and about 5% have mitral valve prolapse (see Ch. 38).
The aortic valve is involved in 20% to 40% of cases. The high inci¬dence of aortic valve involvement probably reflects the increased prev¬alence of aortic stenosis with calcification in Ihe elderly. Until age 60. aortic stenosis with calcification is most commonly caused by rheu¬matic heart disease; from age 60 to 75, a calcified congenital bicuspid valve is most often implicated; and after age 75, degeneration of a nor¬mal valve is the leading cause. The mitral valve is involved in 25% to 70% of endocarditis cases, and both the aortic and mitral valves are involved in about 10% to 25%. Infections involving congenital heart de¬fects other than those of Ihe bicuspid valve occur infrequently in the elderly.
The development of infective endocarditis involves 1 wo events. First is an alteration in the endocardial surface, which then permits the deposi-lion of platelets and fibrin. The resulting thrombus or vegetation most often arises in areas of increased turbulence. Second is transient bacter¬emia, which allows the thrombus to be colonized. The source of bacter¬emia is usually unknown. Sites of primary infection include the mouth, the GU tract (particularly afler procedures involving instrumentation), the GI tract, skin and decubitus ulcers, surgical wounds, and IV cath¬eters.
Bacterial properties—eg. the increased adherence of certain strepto¬coccal and staphylococcal species—-make some organisms more likely than others to cause infective endocarditis. Streptococcus spp are the most common, accounting for 25% to 70% of endocarditis cases, al-Ihough the viridans streptococci arc less prevalent in older than in younger populations. Enterococci, which often inhabit the GU and lower Gl tracts, can account for up to 25%’ of endocarditis cases in el¬derly men. Frequent urinary tract infections and procedures involving instrumentation (especially in men wilh prostate disease) explain the increased frequency of enterococcal bacteremia and endocarditis. S. bovis, a nonenterococcal group D streptococcus, can be isolated in up to 25% of endocarditis cases in persons > 55 yr. Many such cases are associated with underlying and often asymptomatic malignant or premalignant GI lesions, especially colon carcinoma.
Staphylococci account for 20% to 30% of all endocarditis cases in the elderly. The predominant species. Staphylococcus aureus, often causes nosocomial endocarditis, and many cases are discovered only incidentally at autopsy. 5- ep’tdermidis is isolated in < 5% of cases of native valve endocarditis, but in elderly as in younger patients, it is the most common single cause of cases involving prosthetic valves.

occur without asymmetric septal hypertrophy; mitral annular calcifica¬tion may displace the mitral valve anteriorly, producing an outflow gradient. Abnormal ventricular compliance elevates the ventricular di¬astolic pressure, with a resultant increase in left atrial volume and pres¬sure and pulmonary venous congestion. Hypertrophic cardiomyopathy occurs more often in women and has a more favorable prognosis in older patients than in younger ones, with less likelihood of sudden car¬diac death

dissolution of collagen in the elongated chordae tendineae may explain the high incidence of chorda] rupture that often produces life-threaten¬ing heart failure in these patients. Myxomatous degeneration of I he aor¬tic valve often coexists.
Symptoms, Signs, and Laboratory Findings
Presenting symptoms may include disabling chest pain inconsistent with the pain of myocardial ischemia, palpitations or syncope due to arrhythmia, and heart failure secondary to mitral regurgitation. Hearl failure appears to be more common in men. Arrhythmias are common, even in patients with normal ventricular function. The onset of atrial fibrillation may accentuate both mitral and tricuspid valve prolapse and often precipitates hemodynamic deterioration.
The clinical picture includes a midsystolic click or clicks and a late systolic or holosystolic murmur, with characteristic postural variations such as an earlier, louder murmur and earlier and more clicks on assum¬ing the upright position. In contrast to the prominent clicks in younger persons, the mitral regurgitant murmur predominates in elderly pa¬tients. Although patients often have a long history of cardiac murmur, the mitral regurgitation may progressively worsen. Syslemic emboliza¬tion and sudden death may occur.
The ECG often shows abnormalities. The left ventricle may be en¬larged, although the ejection fraction remains normal.
Diagnosis
When chest pain is the predominant finding in mitral valve prolapse, ventricular function is often preserved. Even so, coronary arteriogra¬phy is often needed to differentiate Ihe chest pain of mitral valve pro¬lapse from that of coronary atherosclerosis. Palpitations may be due to both ventricular and supraventricular arrhythmias, and an ambulatory ECG is helpful in documenting Ihe cause. Echocardiography may dif¬ferentiate mitral valve prolapse from other causes of mitral regurgita¬tion and can help assess ventricular chamber size and function.
Treatment
Anticoagulants are given to prevent systemic emboli, which occur predominantly with atrial fibrillation and heart failure. Digitalis is used to control the ventricular response to atrial fibrillation. Hearl failure is managed with digitalis, diuretics, and vasodilators. Mitral valve re¬placement may be indicated for progressive ventricular dilation, which occurs predominantly in men; the surgical risk is acceptable because ventricular function is usually preserved.