Valvular Heart Disease

Major alterations in the preoperative management of patients with valvular heart disease have been made regarding the use of anticoagulant therapy and are now based on the causes of disease. Preoperative and intraoperative

Figure 27-17 First-year mortality rates for patients with acute myocardial infarction (MI) according to subgroup. Pink areas represent patients with ejection fractions of more than 30%; gray areas represent patients with ejection fractions of less than 30%. (The percentages are, by necessity, rough approximations.) CHF, overt congestive heart failure. (Redrawn from Epstein SE, Palmeri ST, Patterson RE: Evaluation of patients after acute myocardial infarction. Indications for cardiac catheterization and surgical intervention. N Engl J Med 307:1487, 1982.)

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Figure 27-18 Relationship of postoperative myocardial ischemia (black bars) and morbid cardiac events (red bars) to hematocrit for 27 high-risk patients undergoing infrainguinal arterial bypass. (Data from Nelson AH, Fleisher LA, Rosenbaum SH: The relationship between postoperative anemia and cardiac morbidity in high risk vascular patients in the ICU. Crit Care Med 21:860, 1993.)

The prognosis and, presumably, the perioperative risk for patients with valvular heart disease depend on the stage of the disease.^{[398] [422]} Although stenotic lesions progress faster than regurgitant lesions do, regurgitant lesions secondary to infective endocarditis, rupture of the chordae tendineae, or ischemic heart disease can be rapidly fatal. Left ventricular dysfunction is common in the late stage of valvular heart disease. Once again, the history and physical examination appear to be the most sensitive and specific indicators of disease and disease stage^{[446] [447]} ( Table 27-36 ).

Preoperative maintenance of drug therapy can be crucial; for example, a patient with aortic stenosis can deteriorate rapidly with the onset of atrial fibrillation or flutter because the atrial contribution to left ventricular filling can be critical in maintaining cardiac output. One of the most serious complications of valvular heart surgery and valvular heart disease before surgery is cardiac arrhythmia. Conduction disorders and chronic therapy with antiarrhythmic and inotropic drugs are discussed elsewhere in this chapter. The reader is referred elsewhere

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Mitral Valve Prolapse

Mitral valve prolapse, perhaps the most frequent valvular abnormality, occurs in 5% to 17% of otherwise healthy people. It is associated with atrioseptal secundum defects,^{[450] [451]} thoracic skeletal abnormalities (as a result of the time of development of these structures), and for unknown reasons, migraine anxiety neurosis and autonomic dysfunction. Hereditary transmission has been proposed to occur through autosomal dominance with reduced expressivity in humans. Mitral valve prolapse is also associated with von Willebrand's syndrome and polycystic kidney disease, and the presence of one condition might call forth a search (by at least history and physical examination) for the other.

Mitral valve prolapse is either asymptomatic or is manifested as palpitations, dyspnea, atypical chest pain, dizziness, syncope, or sudden death. Supraventricular arrhythmias (associated with AV bypass tracts and the pre-excitation syndrome) occur in more than 50% of patients with mitral valve prolapse. Ventricular arrhythmias (usually in surgery) occur in 45% of such patients, bradyarrhythmias in 25%, and sudden death in 1.4%.^{[450] [451]} The frequent occurrence of transient cerebral ischemia has resulted in the chronic use of aspirin or anticoagulants in patients with mitral valve prolapse, and the potential for endocarditis has led to the recommendation for prophylaxis with antibiotics before known bacteremic events^{[450] [451] [452] [453]} and the avoidance of head-up positions and decreased afterload in such patients.

Preoperative Antibiotic Prophylaxis for Endocarditis

Patients who have any form of valvular heart disease, as well as those with intracardiac (ventricular septal or atrial septal defects) or intravascular shunts, should be protected against endocarditis at the time of a known bacteremic event. Endocarditis has occurred in a sufficiently significant number of patients with hypertrophic cardiomyopathy (subvalvular aortic stenosis, asymmetric septal hypertrophy) and mitral valve prolapse to warrant the inclusion of these two conditions in the prophylaxis regimen.

Is endotracheal intubation a bacteremic event? Bacteremia occurs after the following events at these rates: dental extraction, 30% to 80%; brushing of teeth, 20% to 24%; use of oral irrigation devices, 20% to 24%; barium enema, 11%; transurethral prostate resection, 10% to 57%; upper gastrointestinal endoscopy, 8%; nasotracheal intubation, 16% (4 of 25 patients); and orotracheal intubation, 0% (0 of 25 patients).^{[454] [455]} Thus, although bacteremia from orotracheal intubation is rare, we believe that prophylaxis should be given to patients with valvular heart disease before instituting instrumentation of the gallbladder, GI tract, oropharynx, or genitourinary tract. The choice of antibiotic for prophylaxis should be aimed at the most commonly occurring (i.e., most numerous) pathogen^[456] ( Table 27-37 ). Note that these prophylactic regimens should be altered to prevent sepsis after specific surgical procedures^[457] ( Table 27-38 ). Guidelines of the American Heart Association state that all antimicrobial prophylaxis should be started 30 minutes to 1 hour rather than 24 hours before a known bacteremic event so that therapeutic levels are achieved without superinfecting the patient with unusual pathogens.^{[456] [457]}

Cardiac Valve Prostheses and Anticoagulant Therapy and Prophylaxis for Deep Venous Thrombosis

In patients with prosthetic valves, the risk of increased bleeding during a procedure in a patient receiving antithrombotic therapy has to be weighed against the increased risk of thromboembolism caused by stopping the therapy. Common practice in patients undergoing noncardiac surgery with a mechanical prosthetic valve in place is for cessation of anticoagulant therapy 3 days before surgery. This time frame allows the INR to fall to less than 1.5 times normal. The oral anticoagulants can then be resumed on postoperative day 1. Using a similar protocol, Katholi and colleagues found no perioperative episodes of thromboembolism or hemorrhage in 25 patients.^[458] An alternative approach in patients at high risk for thromboembolism is conversion to heparin during the perioperative period. The heparin can then be discontinued 4 to 6 hours before surgery and resumed shortly thereafter. Current prosthetic valves may have a lower incidence, and the risk of heparin may outweigh the benefit in the perioperative setting. According to the American Heart Association/American College of Cardiology guidelines, heparin can usually be reserved for those who have had a recent thrombus or embolus (arbitrarily within 1 year), those with demonstrated thrombotic problems when previously off therapy, those with a Björk-Shiley valve, and those with more than three risk factors (atrial fibrillation, previous thromboembolism, hypercoagulable condition, and mechanical prosthesis).^[459] A lower threshold for recommending heparin should be considered in patients with mechanical valves in the mitral position, in whom a single risk factor would be sufficient evidence of high risk. Subcutaneous low-molecular-weight heparin offers an alternative outpatient approach.^[460] It is appropriate for a surgeon and cardiologist to discuss the optimal perioperative management for such a patient.

Regional anesthetic techniques might be avoided, although this issue is controversial.^{[461] [462] [463] [464] [465] [466] [467] [468] [469] [470] [471] [472] [473] [474] [475] [476]} Many practitioners do not hesitate to use regional anesthesia in the face of prophylaxis for deep venous thrombosis.^{[465] [468] [470] [472]} However, epidural hematoma has been associated with anticoagulant therapy in many reports. Large retrospective reviews of outcome after epidural or spinal anesthesia, or both, during or shortly before initiation of anticoagulant therapy with heparin have not reported neurologic dysfunction related to hematoma formation in any patient.^{[465] [466] [467] [468]} This paucity of damaging epidemiologic evidence, though reassuring, does not reduce the need for frequent evaluation of neurologic function and search for back pain in the perioperative period after regional anesthesia in any patient receiving any clotting function inhibitor, including aspirin.^{[473] [474] [475] [476]} The risk of regional anesthesia concurrent with prophylaxis for deep venous thrombosis with heparin is greater with the use of low-molecular-weight heparin. (Heparin-induced

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Deep venous thrombosis is so common in postoperative patients that almost 1% of postsurgical patients die of fatal pulmonary embolism^[478] ( Table 27-39 ). Because of this high mortality risk, prophylaxis against deep venous thrombosis has attained widespread acceptance; thus, prophylaxis often begins with 5000 U of heparin given subcutaneously 2 hours before surgery.^{[478] [479] [480]} Other trials

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Another problem that can arise is managing a pregnant patient with a prosthetic valve during delivery. It is recommended that warfarin be replaced by subcutaneous heparin during the peripartum period. During labor and delivery, elective induction is advocated with discontinuance of all anticoagulant therapy, as indicated for the particular valve prosthesis (discussed earlier).^[482]

Auscultation of the prosthetic valve should be performed preoperatively to verify normal functioning^[483] ( Fig. 27-19 ). Abnormalities in such sounds warrant preoperative consultation and verification of functioning.