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Otto et al 2020 ACC/AHA Guideline for the Management of Valvular Heart Disease

February 2, 2021 Circulation. 2021;143:e72–e227. DOI: 10.1161/CIR.0000000000000923 e104

CLINICAL STATEMENTS AND GUIDELINES moderate reduction in the transvalvular pressure gradient, but the postdilation valve area rarely exceeds 1.0 cm2. Despite the modest change in valve area, an early symptomatic improvement usually occurs. However, serious acute complications, including acute severe AR, restenosis, and clinical deterioration, occur within 6 to 12 months in most patients. Therefore, in patients with AS, percutaneous aortic balloon dilation is not a substitute for AVR. Some clinicians contend that, despite the procedural morbidity and mortality rates and limited long-term results, percutaneous aortic balloon dilation can have a temporary role in the management of some symptomatic patients, such as those patients with severe AS and refractory pulmonary edema or cardiogenic shock, who might benefit from percutaneous aortic balloon dilation as a “bridge” to TAVI or SAVR. However, this approach is used less frequently given the availability and success of immediate TAVI even in very high-risk patients (Table 14).35–38

4 AORTIC REGURGITATION

4.1 Acute Aortic Regurgitation

Acute aortic regurgitation (AR) may result from abnormalities of the valve, most often endocarditis, or abnormalities of the aorta, primarily aortic dissection. Acute AR may also occur as an iatrogenic complication of a transcatheter procedure or after blunt chest trauma. The acute volume overload on the LV usually results in severe pulmonary congestion, as well as a low forward cardiac output. Urgent diagnosis and rapid intervention are lifesaving.

4.1.1 Diagnosis of Acute AR

TTE or TEE is indispensable in confirming the presence, severity, and etiology of acute AR; determining whether there is rapid equilibration of the aortic and LV diastolic pressures; visualizing the aortic root; and evaluating LV size and systolic function.1,2 A short deceleration time on the aortic flow velocity curve and early closure of the mitral valve are indicators of markedly elevated LV end-diastolic pressure. A pressure half-time of <300 ms on the AR velocity curve indicates rapid equilibration of the aortic and LV diastolic pressures. The degree of holodiastolic flow reversal in the aortic arch, in comparison with the forward systolic flow, provides a quick semiquantitative estimate of regurgitant fraction. Acute severe AR caused by aortic dissection is a surgical emergency. CT imaging is the primary approach for diagnosis of acute aortic dissection because it is highly accurate and continuously available at most medical centers. MRI is rarely used in the acute setting because of patient instability. TEE may be used when CT imaging is unavailable and is helpful in intraoperative assessment of aortic valve function before and after the surgical intervention. The sensitivity and specificity of TTE for diagnosis of Type A3 aortic dissection are only 60% to 80%, whereas TEE has a sensitivity of 98% to 100% and a specificity of 95% to 100%. Angiography should be considered only when the diagnosis cannot be determined by noninvasive imaging or when the differential diagnosis is an acute coronary syndrome.

4.1.2 Intervention for Acute AR

In patients with acute severe AR resulting from IE or aortic dissection, medical therapy to reduce LV afterload may allow temporary stabilization, but surgery should not be delayed, especially if there is hypotension, pulmonary edema, or evidence of low flow.1–4 Intra-aortic balloon counterpulsation is contraindicated in patients with acute severe AR.5 Beta blockers are often used in treating aortic dissection. However, these agents should be used very cautiously, if at all, for other causes of acute AR because they will block the compensatory tachycardia and could precipitate a marked reduction in blood pressure.

4.2 Stages of Chronic AR

The most common causes of chronic severe AR in the United States and other high-income countries are BAV disease and primary diseases of the ascending aorta or the sinuses of Valsalva. Rheumatic heart disease is the leading cause of AR in many low- to middle-income countries. With calcific valve disease, regurgitation often accompanies AS, but the degree of regurgitation usually is mild to moderate, not severe. In most patients with AR, the disease course is chronic and slowly progressive, with increasing LV volume overload and LV adaptation via chamber dilation and hypertrophy. Management of patients with AR depends on an accurate diagnosis of the cause and stage of the disease process. Table  15 shows the stages of AR, ranging from patients at risk of AR (Stage A) or with progressive mild to moderate AR (Stage B) to severe asymptomatic (Stage C) and symptomatic (Stage D) AR. Each of these stages is defined by valve anatomy, valve hemodynamics, severity of LV dilation, and LV systolic function, as well as by patient symptoms.

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