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(49%), followed by stenosis (21%) and combined regurgitation/ stenosis (30%). The incidence of both aortic and mitral bioprosthesis deterioration requiring reintervention is 20% to 30% at 10 years and over 50% at 15 years, although it is important to note that the clinical manifestations are more often chronic than acute. Acute prosthetic valve dysfunction due to thrombosis or endocarditis can also manifest as thromboembolism (cerebral or peripheral).

Diagnosis

Normally functioning prosthetic valves are associated with various opening and closing clicks and systolic and occasionally diastolic ﬂow murmurs. A new or changing murmur may therefore signal a pathophysiologic alteration in prosthetic valve function. In addition, the absence or damping of normal valve clicks that are characteristic of mechanical prostheses also suggests abnormalities in valve function.

As part of the initial evaluation, identiﬁcation of the class, type, and model of the implanted valve and the date of implantation is extremely important. The chest radiograph can be invaluable in assessing for the presence of heart failure and may provide conﬁrmatory radiologic evidence as to the type of valvular prosthesis that is in place.78 The ECG may show signs of LV overload but these ﬁndings are not speciﬁc in detecting prosthetic valve dysfunction, as they may antedate valve replacement. Anemia in association with an elevated serum lactic dehydrogenase level greater than 600 IU, suggesting hemolysis is virtually never found in a normal functioning prosthesis and should always raise the suspicion of a perivalvular leak and destruction of red blood cells due to increased shear stress.

Echocardiography is an essential tool in the evaluation of prosthetic valve dysfunction.80 It serves the dual purpose of identifying the etiology of the valve abnormality and assessing LV function. Doppler echocardiography to assess the color ﬂow, pulsed wave, and continuous wave Doppler imaging should be performed to further interrogate the prosthesis. Measurements should be taken from the average of three consecutive cardiac cycles for patients in sinus rhythm or a minimum of ﬁve cardiac cycles if the patient is in an irregular rhythm. Some caveats with the use of echocardiography include the familiarity of the echocardiography reader with normal prosthetic jets and the real-time hemodynamics of the patient that may affect Dopplerderived values. A skilled echocardiography reader should be familiar with the appearance of normal transprosthetic jets that arise due to the design of the prostheses to prevent an erroneous diagnosis of pathologic regurgitation or stenosis. Additionally, Doppler-derived hemodynamic parameters, such as mean gradient and peak velocity, are dependent on the ﬂow state. For example, these hemodynamic parameters may be elevated in high ﬂow states—such as tachycardia, hyperthyroidism, or renal disease— rather than from pathologic obstruction or regurgitation.

Color Doppler ﬂow mapping has several important applications in prosthetic valve disease: (1) directing continuous-wave Doppler cursor parallel to the stenotic ﬂow jet, allowing more accurate estimation of transprosthetic velocities and gradients (2) semiquantitative evaluation of prosthetic valve regurgitation, which has been shown to correlate well with angiographically

;

derived measurements

82,83

; and (3) differentiating valvular from perivalvular leaks.81 The evaluation for prosthetic valve dysfunction uses Doppler-derived variables, including velocity, acceleration time, pressure gradient, time velocity integral (TVI), Doppler velocity index (DVI), and effective oriﬁce area (EOA). The normal values for velocities and pressures vary based on the prosthetic valve location, type, and size. Expected values for different valve types can be found in the 2009 American Society of Echocardiography (ASE) Prosthetic Valve guidelines.

Continuous-wave Doppler imaging is effective in assessing

valvular stenosis by virtue of the modiﬁed Bernoulli equation:

Pressure Velocity=×4

The transvalvular velocities measured by Doppler echocardiography correlate well with invasive measures in patients with native valve disease and after valve replacement.85 When the valve oriﬁce is smaller or more stenotic, the acceleration and velocity increases to maintain the same stroke volume. Using the Doppler-measured velocities proximal and distal to the valve, the pressure gradient or difference can be calculated. Although transvalvular pressure differences are proportional to the degree of stenosis, variables such as heart rate, contractility, cardiac output, and the size and type of prosthesis can alter the measured gradient.

The dynamic ﬂow velocities can also be plotted against the ejection time axis to provide the TVI, a representation of the distance the blood travels with each cardiac cycle. The DVI is a dimensionless ratio of proximal velocity in the LV outﬂow tract to that of ﬂow velocity through the prosthesis. It is not dependent on the ﬂow conditions through the valve, whereas the gradient and velocity are. In addition, the DVI is less dependent on the valve size. A DVI less than 0.25 is highly suggestive of signiﬁcant valve obstruction.84 The EOA can be calculated by dividing the left ventricular stroke volume by the TVI using the continuity equation. Since it is dependent on the size of the prosthetic valve, there are different reference values for the type of valve. In general, an EOA less than 0.8 cm2 is concerning for signiﬁcant stenosis. In patients with normal or low EOA, prosthetic-patient mismatch or a pathologic valve obstruction is highly suspected, particularly if the mean gradient is elevated. Prosthesis-patient mismatch refers to the condition in which the effective prosthetic valve area is less than the normal human valve after insertion into the patient. Obstruction is often due to a pannus ingrowth, thrombus, or vegetation. If the EOA index is elevated with a high mean gradient, the concern for prosthetic valve regurgitation is heightened. Although prosthetic valves are generally inherently stenotic, physiologic regurgitation can also be seen in mechanical valves. Pathologic regurgitation that is central valvular may be secondary to degeneration, vegetation, or leaﬂet malfunction; perivalvular regurgitation is concerning for dehiscence, abscess, or improper seating of the prostheses. Various cutoffs have been proposed for the location and type of prostheses.

An important phenomenon to be mindful of when evaluating mean gradients in prosthetic valves is pressure recovery. When blood is pumped through the aortic prosthetic valve, the lowest pressure and highest velocity is at the vena contracta, which is a few millimeters from the prosthesis outﬂow oriﬁce. As the blood is propelled forward through the aorta, the pressure recovers

CHAPTER 26 Acute Presentations of Valvular Heart Disease 271

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as the velocity decreases. Thus, the pressure gradient (LV pressure–aortic pressure) is dependent on where the velocity is interrogated in reference to the vena contracta. For smaller mechanical bileaﬂet valves, a higher mean gradient is often considered to be normal owing to pressure recovery. Clinically, it is the net pressure gradient rather than the maximal pressure gradient that correlates with the true hemodynamic burden on

the LV.

It should also be remembered that there is a wide variation in valvular gradients depending on the class, type, and model of the valve. Therefore patients with newly implanted valves should have a full TTE study, including comprehensive Doppler assessment, to evaluate the prosthesis as a baseline for future follow-up. The 2014 American Heart Association/American College of Cardiology (AHA/ACC) guidelines recommend that the initial TTE be obtained 6 weeks to 3 months after valve implantation.88 Repeat TTE is recommended in patients with prosthetic heart valves if there is a change in clinical signs or symptoms suggesting valve dysfunction. Compelling evidence to support a particular strategy in timing of echocardiographic follow-up for asymptomatic patients with prosthetic heart valves is lacking. Current guidelines do not recommend further echocardiographic testing after the initial postoperative period in asymptomatic patients with mechanical valves. Annual TTE in asymptomatic patients with a bioprosthetic valve after the ﬁrst 10 years even in the absence of a change in clinical status is reasonable, as the likelihood of valve dysfunction is more common at this time. In cases in which valve function is difﬁcult to visualize owing to artifact or acoustic shadowing on a TTE, TEE, ﬂuoroscopy, and/or gated CT imaging may be warranted.

When transthoracic imaging is limited secondary to reverberatory artifacts caused by metallic components of a mechanical valve or technically difﬁcult echocardiographic windows, TEE is a useful adjunctive tool.

90–96

Because imaging is performed without intervening cardiac structures, excellent delineation of valvular anatomy and function may be obtained. This is particularly true in the case of the mitral valve because the esophageal window is not obstructed by the metallic valve components. In addition, several studies have suggested that TEE may, in fact, be more sensitive and speciﬁc than TTE in the evaluation of partial valve thrombosis, aortic ring abscess,

97–99

100

perivalvular leaks,95 Starr-Edwards prosthesis

prosthetic valve endocarditis with

function,94 and bioprosthetic valve degeneration.96 TEE may also be appropriate when TTE ﬁndings are not consistent with the observed clinical syndrome. However, it should be emphasized that the combined approach of using TTE with TEE facilitates a more complete evaluation of LV function.

In the case of acute prosthetic valve dysfunction with heart failure, right heart catheterization is essential for continuous hemodynamic monitoring and for helping to deﬁne therapeutic interventions. Because echocardiography has, in large part, replaced traditional catheterization measurements for valvular insufﬁciency and stenosis, cardiac catheterization is withheld unless the available echocardiographic data are inconclusive or there is a suspicion of signiﬁcant coronary artery disease. In some cases, simple ﬂuoroscopy may be used to identify prosthetic valve dysfunction and assess the effects of thrombolytic

therapy on abnormalities caused by clots that affect valve function.

101–103

Treatment

Congestive Heart Failure. Therapy for acute prosthetic valve

dysfunction depends on the type and severity of hemodynamic abnormality, the valve involved, and the underlying etiology. If the valve becomes obstructed acutely, the clinical presentation is likely to be dramatic, with syncope and death in the absence of immediate surgical intervention. On the other hand, stenotic lesions that develop more gradually present as progressive heart failure and a low cardiac output state. Medical management consists of reducing LA pressure and maximizing ventricular performance with inotropic agents. Acute regurgitant lesions are managed according to the guidelines outlined in the sections on treatment for aortic, mitral, and tricuspid regurgitation. Usually, this will involve a combination of vasodilators, diuretics, and inotropic support. Deﬁnite therapy usually involves reoperation and replacement of the dysfunctional valve. The mortality risk for reoperation will depend primarily on the preoperative functional class, the underlying etiology of the valve dysfunction (endocarditis and valve thrombosis carrying the highest risk) and the need for emergency surgery. Valve surgery is recommended in severe prosthetic valve stenosis and severe prosthetic valve or paraprosthetic valve regurgitation with heart failure or intractable hemolysis. For high operative risk yet symptomatic patients with bioprosthetic aortic valve stenosis or regurgitation, a transcatheter valve-in-valve procedure is now included as a class IIa recommendation in the focused update of the 2017 AHA/ACC Valvular Heart Disease guidelines. Percutaneous repair is suggested for patients with severe perivalvular regurgitation with intractable hemolysis and New York Heart Association (NYHA) class III or IV heart failure who are at high risk from surgery.

Prosthetic Valve Endocarditis. Speciﬁc management of

prosthetic valve endocarditis (PVE) includes obtaining blood cultures and initiating empiric antibiotic therapy. Because there is a fairly well-deﬁned difference between the pathophysiology and type of organisms responsible for early and late PVE, the initial choice of antibiotics will depend on the time of presentation relative to the date of surgical valve replacement. In early infection within 2 months of implantation, the new valve apparatus has not endothelialized, allowing microorganisms direct access to the new structures either from direct intraoperative contamination or hematogenous spread. Most common pathogens are nosocomial, including S. aureus and coagulase-negative staphylococci. In late infections, deﬁned as 2 months or more after implantation, the valve apparatus has become endothelialized; thus, the pathogenesis of endocarditis is similar to that of native valve endocarditis. The most common pathogens in late infections are streptococci and S. aureus.

In addition to progressive heart failure, PVE may also be complicated by embolic phenomena or perivalvular leak (with or without hemolytic anemia). As progressive damage may advance rapidly in patients with prosthetic valves who have these complications, it is appropriate to obtain blood cultures and

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initiate empiric antibiotic therapy. In the setting of aortic prosthetic valvular endocarditis, the development of new atrioventricular conduction delay is speciﬁc for the presence of a valve ring abscess.79 Invariably, the vast majority of patients with PVE will require valve replacement. Based on the 2015 AHA scientiﬁc statement regarding infective endocarditis, early surgery during the initial hospitalization for antibiotic therapy is recommended for patients with PVE with one or more of the following: signs or symptoms of heart failure from valvular dysfunction, heart block or valve abscess due to perivalvular invasion, PVE caused by fungi or a highly resistant organism, such as S. aureus, or persistent bacteremia despite appropriate therapy.

104

Transcatheter heart valve endocarditis is an emerging complication of percutaneous valve replacement. Early TAVR-related PVE has been reported at a rate of 0.3% to 0.4% per patient year.

105

Complications include heart failure, perivalvular invasion of the infection, embolic events, and valvular dysfunction, such as stenosis or regurgitation. There is limited evidence regarding optimal treatment for TAVR-related PVE and surgical indications that is often adapted from PVE on surgically placed valves and made on an individual basis.

Prosthetic Valve Thrombosis. Although valvular obstruction

may occasionally be secondary to bacterial vegetations, they are more commonly the result of pannus ingrowth or thrombus formation. Subclinical asymptomatic prosthetic valve thrombosis (PVT) is likely more common than symptomatic PVT; however, there are limited data on the incidence and clinical signiﬁcance of subclinical PVT. The incidence of PVT with currently available mechanical devices varies from 0.3% to 1.3% with a higher rate of approximately 6% in patients with mechanical prostheses who have had subtherapeutic anticoagulation. Mitral mechanical PVT is more common than aortic mechanical PVT. The incidence of bioprosthetic PVT is less well deﬁned. Although a major risk factor for PVT is inadequate anticoagulation, approximately 40% of patients have adequate prothrombin times at the time of presentation.

106

This may be explained by the fact that PVT is a complex process that consists of a signiﬁcant component of ﬁbrous tissue ingrowth with associated secondary thrombosis.

PVT may present acutely with heart failure or more indolently with slowly progressive symptoms of dyspnea and fatigue. A high level of suspicion must be maintained in any patient with a valvular prosthesis with nonspeciﬁc cardiac symptoms. TTE provides assessment of hemodynamic severity, whereas CT imaging or ﬂuoroscopy is often used to delineate valve motion and clot burden. TEE is useful in measuring thrombus size (Videos

26.5 and 26.6). Although the mortality rate for reoperation is variable between reports, ranging from 4.5% to 35%, it tends to be high; there is a correlation between risk and advanced functional class.

Options for the management of PVT include medical or surgical therapy. The 2017 focused update of the AHA/ACC valvular heart disease guidelines now includes a class IIa recommendation for initiation of vitamin K antagonist agents in patients with suspected or conﬁrmed bioprosthetic valve thrombosis who are hemodynamically stable based on case series data. According to the 2014 AHA/ACC valvular heart disease guidelines, emergent

surgery is a class I recommendation for patients with left-sided prosthetic valve thrombosis with NYHA class III to IV symptoms. Surgery is a class IIa recommendation for left-sided prosthetic valve thrombosis that is mobile or large (>0.8 cm). This is mostly based on a meta-analysis of seven observational studies that demonstrated that surgery for left-sided PVT with severe functional impairment was associated with signiﬁcantly lower rates of thromboembolism, major bleeding, and recurrent PVT compared to ﬁbrinolytic therapy. Mortality rates and complete restoration of valve function was not signiﬁcantly different. Fibrinolytic therapy for persistent valve thrombosis despite intravenous heparin therapy is a class IIa recommendation for right-sided prosthetic valve thrombosis or left-sided prosthetic valve thrombosis with recent onset of symptoms (<14 days), stable thrombus (<0.8 cm2), and/or NYHA class I/II symptoms. Streptokinase or tissue plasminogen activator (tPA) is recommended for ﬁbrinolytic therapy; urokinase is less effective. Complications of left-sided PVT ﬁbrinolysis include major bleeding, systemic embolization, recurrent PVT, and death. The degree of risk for thromboembolism and bleeding is directly related to thrombus size, with thrombus areas greater than 0.8 cm2 associated with a higher risk.

TRICUSPID REGURGITATION

In general, the hemodynamic impact of acute tricuspid regurgitation is less signiﬁcant than that of acute left-sided valvular lesions. More commonly, persistent, severe, chronic tricuspid regurgitation results in salt and water retention leading to peripheral edema, ascites, and congestive hepatomegaly. However, acute tricuspid regurgitation can lead to massive RV volume overload, causing signiﬁcant reduction in LV ejection fraction due to paradoxic early systolic septal motion that results from the severe volume overload of the RV. be pronounced at the time of initial presentation, many patients with the onset of acute severe tricuspid regurgitation can be effectively managed with a combination of diuretics and inotropic agents, provided that pulmonary arterial pressure remains normal and RV function is preserved. Once stabilized, the long-term prognosis of these patients tends to be favorable. In general, the clinical presentation, response to medical therapy, and underlying pathology determine the need for surgical intervention.

Etiology

It should be emphasized that isolated, acute tricuspid regurgitation is a relatively uncommon medical emergency. The chronic form of tricuspid regurgitation predominates and usually results from annular dilation secondary to left-sided valvular pathology, severe LV dysfunction, or pulmonary hypertension. In the current era, infective endocarditis remains the most common cause of acute tricuspid regurgitation and is almost exclusively a disease of intravenous drug users. the valve lesion, these individuals frequently develop ruptured chords or leaﬂet perforation. Occasionally, tricuspid regurgitation can be caused by a large, healed vegetation that impairs leaﬂet apposition. Rarer causes of acute tricuspid regurgitation include nonpenetrating chest trauma

108

Although hemodynamic instability may

109

Despite antibiotic sterilization of

110,111

and RV infarction.

112,113

107

With

CHAPTER 26 Acute Presentations of Valvular Heart Disease 273

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the growing number of cardiac transplant recipients, an iatrogenic form of tricuspid regurgitation has been recognized with increasing frequency.

114–117

Transplant patients undergo repeated endomyocardial biopsies for evaluation of cardiac allograft rejection and, occasionally, the bioptome may inadvertently damage the tricuspid valve chordae or leaﬂet, resulting in acute tricuspid regurgitation.

Clinical Presentation

The physical ﬁndings in acute tricuspid regurgitation are dependent, in part, on the severity of the RV volume overload. In the case of papillary muscle rupture or RV infarction, there may be hypotension and cardiovascular collapse. Most patients, however, maintain blood pressure within the normal range and typically demonstrate ﬁndings consistent with right-sided heart failure. There is usually a prominent “v” wave visible in the jugular venous pulse and a holosystolic murmur along the left sternal border. The tricuspid regurgitation murmur increases in intensity with inspiration, a ﬁnding that differentiates it from mitral regurgitation. An S3 gallop originating from the RV can be heard; abdominal examination may reveal a large and pulsatile liver. In general, peripheral stigmata of infective endocarditis are absent when the tricuspid valve is affected and, if present, suggest paradoxic emboli or additional, left-sided valvular lesions. In the case of intravenous drug users, track marks and evidence of “skin popping” may be seen.

Fig. 26.13 Four-chamber transthoracic echocardiogram shows a

ﬂail tricuspid valve (arrow). RA, Right atrium; RV, right ventricle.

Diagnosis

The diagnostic modality of choice for evaluating acute tricuspid regurgitation is two-dimensional and Doppler echocardiogra-

118

phy.

The echocardiogram provides structural information about the tricuspid valve, including detection of vegetations. In addition, the severity of tricuspid regurgitation and RV dysfunction can be assessed. Most important, pulmonary artery pressures can be estimated using the modiﬁed Bernoulli equation:

where PAS is pulmonary artery systolic pressure, RAP is right atrial pressure measured by physical examination [5 cm + jugular venous pressure (cm above clavicle)], and V is the peak velocity of the tricuspid regurgitation jet measured by continuous-wave Doppler. tory for assessing tricuspid valve structure and RV function (Figs.

26.13 and 26.14). An important caveat, though, is that when the

RV fails, ﬂow directed into the pulmonary artery and backwards into the right atrium may be reduced so that the severity of pulmonary hypertension or tricuspid regurgitation may be underestimated. TEE may not offer any signiﬁcant diagnostic advantage over TTE. In a prospective study by San Román and colleagues, TTE was equivalent to TEE in the diagnosis of tricuspid valve infective endocarditis; however, the relationship of the vegetation to the leaﬂet was better characterized by TEE.

block. If the tricuspid regurgitation has been long standing, there may be ECG criteria for RV hypertrophy. RV infarction with acute tricuspid regurgitation rarely occurs in isolation and typically presents in conjunction with inferior MI, which can be diagnosed

119

In general, transthoracic echocardiography is satisfac-

120

The ECG in cases of trauma may show right bundle branch

Fig. 26.14 Apical transthoracic echocardiogram with color Doppler,

a ﬂail tricuspid valve, and associated tricuspid regurgitation (arrow). RV, Right ventricle.

by the characteristic ST segment elevation in leads II, III, and aVF. The presence of ST segment elevation in the right-sided lead V4R conﬁrms the diagnosis of an RV infarct and suggests that the patient may be at high risk for complications.

121

The chest radiograph may show signs of cardiomegaly that represent RV and right atrial (RA) enlargement. The presence of cavitary septic pulmonary emboli may also be seen with tricuspid valve endocarditis. As noted, blood cultures are an essential component of the diagnostic workup for patients with suspected infective endocarditis. In patients with a history of intravenous drug use, staphylococcal organisms are the predominant isolate.

Right heart catheterization can be extremely helpful in conﬁrming the diagnosis of pure tricuspid regurgitation and ruling out signiﬁcant LV abnormalities. The presence of a large “v” wave in the RA tracing with concomitant elevation in mean RA pressure usually signiﬁes the presence of signiﬁcant tricuspid regurgitation. In addition, if the pulmonary artery and capillary wedge pressures are normal, the tricuspid regurgitation is likely to be related to primary dysfunction of the valvular apparatus and not secondary to left-sided heart dysfunction or pulmonary hypertension.

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apparatus. Even with complete valve excision, many of these

Treatment

The management strategy for acute tricuspid regurgitation should be focused primarily on medical therapy. Most patients can be effectively treated with a diuretic alone or in combination with an inotropic agent, such as dobutamine. Milrinone, another inotropic agent, may be used as well, particularly in patients who have evidence of pulmonary hypertension. In rare instances of acute massive tricuspid regurgitation, the patient who is refractory to medical therapy may require immediate surgical intervention. Whenever possible, tricuspid valve repair, often with ring annuloplasty, is preferred over valve replacement. However, when valve replacement is required, a bioprosthetic valve is often used as there is a high incidence of valve thrombosis when mechanical valves are implanted in the tricuspid position. In the case of tricuspid regurgitation related to infective endocarditis, the decision to implant a prosthetic valve becomes even more complex. Because many of these patients are young, noncompliant, and often return to intravenous drug use, their risks for adverse events—whether self-induced or iatrogenic—are signiﬁcant. The operative mortality for reoperation, particularly for recurrent prosthetic valve endocarditis, can be extremely high. Furthermore, if a bioprosthesis is used, the risk of valve failure over time is higher because of the younger age of the intravenous drug–using population. The choice of a mechanical valve for durability is also fraught with complications from both the inherently higher thrombotic risk despite anticoagulation and the general trend of medication noncompliance among these patients. Although treatment cannot be generalized for the intravenous drug–use population, these recurring problems have fostered the development of several unique surgical approaches. These options include complete valve excision with no prosthetic replacement, and “vegectomy,” bacterial vegetation with preservation of the valvulochordal

123

valve repair after sterilization of the infection,

125

which refers to isolated resection of the

patients may continue to do well, with minimal symptoms of right-sided heart failure. This is particularly true when the pulmonary vascular resistance is normal and RV function is preserved. Naturally, any management plan for infective endocarditis must include appropriate antibiotic coverage for an adequate period of time.

The treatment of tricuspid regurgitation secondary to an inferior MI with RV involvement is revascularization. The type of revascularization procedure will depend on the nature of the coronary anatomy, extent of atherosclerotic disease, myocardial territory at risk, and LV function.

CONCLUSION

122

Acute heart failure secondary to valvular dysfunction remains an extremely difﬁcult clinical dilemma from the standpoint of both diagnosis and treatment. Since the underlying pathophysiology determines the clinical course, expeditious treatment with appropriate diagnostic testing is of paramount importance. In most cases of acute heart failure secondary to valvular disease, both echocardiography and pulmonary artery catheterization are invaluable tools that allow the clinician to determine the severity of the lesion as well as underlying cardiac function, assess the patient’s hemodynamic status, and reach decisions regarding the best management strategy. Providers treating patients with acute valvular dysfunction must not only understand the pathophysiology of the disease but also be cognizant of the limitations of medical therapy. As surgical intervention represents the most deﬁnitive intervention, early cardiothoracic surgical consultation is a critical step in the management algorithm of these often desperately ill individuals.

124

The full reference list for this chapter is available at

ExpertConsult.com.

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REFERENCES

1. Dervan J, Goldberg S. Acute aortic regurgitation: pathophysiology and management. Cardiovasc Clin. 1986;16:281–288.

2. Freedman LR. The pathogenesis of infective endocarditis. J Antimicrob Chemother. 1987;20(supplA):1.

3. Slater EE, DeSanctis RW. The clinical recognition of dissecting aortic aneurysm. Am J Med. 1976;60:625.

4. Hirst AE, Gore I. The etiology and pathology of aortic regurgitation. In: Doroghazi RM, Slater EE, eds. Aortic Dissection. New York: McGraw-Hill Book; 1983:13.

5. Hamirani YS, Dietl CA, Voyles W, et al. Acute aortic regurgitation. Circulation. 2012;126:1121–1126.

6. Mokadam NA, Stout KK, Verrier ED. Management of Acute Regurgitation in Left-Sided Cardiac Valves. Tex Heart Inst J. 2011;38(1):9–19.

7. Robicsek F, Thubrikar MJ. Hemodynamic considerations regarding the mechanism and prevention of aortic dissection. Ann Thorac Surg. 1994;58:1247.

8. Welch GH, Braunwald E, Sarnoff SJ. Hemodynamic effects of quantitatively varied experimental aortic regurgitation. Circ Res. 1957;5:546.

9. Wigle ED, Labrosse CJ. Sudden, severe aortic insufﬁciency. Circulation. 1965;32:708.

10. Perloff JK. Acute severe aortic regurgitation: recognition and management. J Cardiovasc Med. 1983;8:209.

11. Wong M. Diastolic mitral regurgitation: hemodynamic and angiographic correlation. Br Heart J. 1969;31:468.

12. Pridie RB, Benham R, Oakley CM. Echocardiography of the mitral valve in aortic valve disease. Br Heart J. 1971;33:296.

13. Flint A. The mitral cardiac murmurs. Am J Med Sci. 1886; 91:27.

14. Fortuin NJ, Craige E. On the mechanism of the Austin Flint murmur. Circulation. 1972;45:558.

15. Zoghbi WA, Enriquez-Sarano M, Foster E, et al. Recommendation for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;16:777.

16. Carpenter JL. Peri-valvular extension of infection in patients with infectious endocarditis. Rev Infect Dis. 1991;13:127.

17. Nienaber CA, von Kodolitsch Y, Nicolas V, et al. The diagnosis of thoracic aortic dissection by non-invasive imaging procedures. N Engl J Med. 1993;328:1.

18. Baliga RR, Nienaber CA, Bossone E, et al. The role of imaging in aortic dissection and related syndromes. J Am Coll Cardiol Img. 2014;7(4):406–424.

19. Shiga T, Wajima Z, Apfel C, et al. Diagnostic accuracy of transesophageal echocardiography, helical computed tomography, and magnetic resonance imaging for suspected thoracic aortic dissection. Arch Intern Med. 2006;166:1350.

20. Rahimtoola SH. Recognition and management of acute aortic regurgitation. Heart Dis Stroke. 1993;2:217.

21. Cohn JN, Burke LP. Diagnosis and treatment: drugs ﬁve years later: nitroprusside. Ann Intern Med. 1979;91:752.

22. Akhtar N, Mikulic E, Cohn JN, et al. Hemodynamic effect of dobutamine in patients with severe heart failure. Am J Cardiol. 1975;36:202.

23. Wilson WR, Thandroyen FT. Infective endocarditis. In: Willerson JT, Cohn JN, eds. Cardiovascular Medicine. New York: Churchill Livingstone; 1995:240.

24. Lalani T, Cabell CH, Benjamin DK, et al. Analysis of the Impact of Early Surgery on In-hospital Mortality of Native Valve Endocarditis: Use of Propensity Score and Instrumental Variable Methods to Adjust for Treatment Selection Bias. Circulation. 2010;121(8):1005–1013.

25. Pape LA, Awais M, Woznicki EM, et al. Presentation, Diagnosis, and Outcomes of Acute Aortic Dissection: 17-Year Trends From the International Registry of Acute Aortic Dissection. J Am Coll Cardiol. 2015;66:350–358.

26. Kennedy KD, Nishimura RA, Holmes DR Jr, et al. Natural history of moderate aortic stenosis. J Am Coll Cardiol. 1991;17:313.

27. Stott DK, Marpole DGF, Bristow JD, et al. The role of left atrial transport in aortic and mitral stenosis. Circulation. 1970;41:1031.

28. Marcus ML, Doty DB, Hiratzka LF, et al. Decreased coronary reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries. N Engl J Med. 1982;307:1362.

29. Morton BC. Natural history and management of chronic aortic valve disease. Can Med Assoc J. 1982; 126:477.

30. Forssell G, Jonasson R, Orinius E. Identifying severe aortic valvular stenosis by bedside examination. Acta Med Scand. 1985;218:397.

31. Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease. J Am Coll Cardiol. 2017.

32. Gregoric ID, Loyalka P, Radovancevic R, et al. TandemHeart as a rescue therapy for patients with critical aortic valve stenosis. Ann Thorac Surg. 2009;88:1822–1826.

33. Martinez CA, Singh V, Londoño JC, et al. Percutaneous retrograde left ventricular assist support for interventions in patients with aortic stenosis and left ventricular dysfunction. Catheter Cardiovasc Interv. 2012;80(7):1201–1209. doi:10.1002/ ccd.24303.

34. Généreux P, Head SJ, Hahn R, et al. Perivalvular leak after transcatheter aortic valve replacement: the new Achilles’ heel? A comprehensive review of the literature. J Am Coll Cardiol. 2013;61:1125–1136.

35. Sponga S, Perron J, Dagenais F, et al. Impact of residual regurgitation after aortic valve replacement. Eur J Cardiothorac Surg. 2012;42:486–492.

36. Gilard M, Eltchaninoff H, Iung B, et al. Registry of transcatheter aortic-valve implantation in high-risk patients. N Engl J Med. 2012;366:1705–1715.

37. Kapadia SR, Svensson L, Tuzcu EM. Successful percutaneous management of left main trunk occlusion during percutaneous aortic valve replacement. Catheter Cardiovasc Interv. 2009;73(7):966–972.

38. Martinez CA, Singh V, Heldman AW, O’Neill WW. Emergent use of retrograde left ventricular support in patients after transcatheter aortic valve replacement. Catheter Cardiovasc Interv. 2013;82(2):E128–E132.

39. Cowger J, Pagani FD, Haft JW, et al. The Development of Aortic Insufﬁciency in LVAD Supported Patients. Circulation Heart failure. 2010;3(6):668–674.

40. Westaby S, Bertoni GB, Clelland C, Nishinaka T, Frazier OH. Circulatory support with attenuated pulse pressure alters human aortic wall morphology. J Thorac Cardiovasc Surg. 2007;133(2):575–576.

274.e2 PART IV Noncoronary Diseases: Diagnosis and Management

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41. D’Ancona G, Pasic M, Buz S. TAVI for pure aortic valve insufﬁciency in a patient with a left ventricular assist device. Ann Thorac Surg. 2012;93:e89–e91.

42. Santini F, Forni A, Dandale R. First successful management of aortic valve insufﬁciency associated with Heartmate II left ventricular assist device support by transfemoral Corevalve implantation: The Columbus egg? JACC Cardiovasc Interv. 2012;5:114–115.

43. Parikh KS, Mehrotra AK, Russo MJ. Percutaneous transcatheter aortic valve closure successfully treats left ventricular assist device-associated aortic insufﬁciency and improves cardiac hemodynamics. JACC Cardiovasc Interv. 2013;6:84–89.

44. Wei JY, Hutchins GM, Bulkley BH. Papillary muscle rupture in fatal acute myocardial infarction. Ann Intern Med. 1979;90:149.

45. Burch GE, DePasquale NP, Phillips JH. Clinical manifestations of papillary muscle dysfunction. Arch Intern Med. 1973;12:58.

46. DeBusk RF, Harrison DC. The clinical spectrum of papillary muscle disease. N Engl J Med. 1969;281:1458.

47. Pearson AC, St Vrain J, Mrosek D, et al. Color Doppler echocardiographic evaluation of patients with a ﬂail mitral leaﬂet. J Am Coll Cardiol. 1990;15:564.

48. Luther RR, Meyers SN. Acute mitral insufﬁciency secondary to ruptured chordae tendineae. Arch Intern Med. 1974;134:568.

49. John S, Bashi VV, Jairaj PS, et al. Closed mitral valvotomy: early results and long-term follow-up of 3724 consecutive patients. Circulation. 1983;68:891.

50. Harrison JK, Wilson JS, Hearne SE, et al. Complications related to percutaneous transvenous mitral commissurotomy. Cathet Cardiovasc Diagn. 1994;S2:52.

51. Feldman T, Carrol JD, Herrmann HC, et al. Mitral regurgitation (not restenosis) is the most frequent indication for valve replacement after balloon mitral valvotomy. J Am Coll Cardiol. 1995;64A:910.

52. Braunwald E, Welch GH Jr, Sarnoff SJ. Hemodynamic effects of quantitatively varied experimental mitral regurgitation. Circ Res. 1957;5:539.

53. Roberts WC, Braunwald E, Morrow AG. Acute severe mitral regurgitation secondary to ruptured chordae tendineae: clinical, hemodynamic and pathologic considerations. Circulation. 1966;3:58.

54. Linhart JW, Hildner FJ, Barold SS, et al. A hemodynamic study of acute mitral valve regurgitation in man. Chest. 1970;57:22.

55. Ronan JA, Steelman RB, DeLeon AC, et al. The clinical diagnosis of acute severe mitral insufﬁciency. Am J Cardiol. 1971;27:284.

56. Dugall JC, Pryor R, Blount SG Jr. Systolic murmur following myocardial infarction. Am Heart J. 1974;87:577.

57. Sanders CA, Armstrong PW, Willerson JT, et al. Etiology and differential diagnosis of acute mitral regurgitation. Prog Cardiovasc Dis. 1971;14:129.

58. Antman EM, Angoff GH, Sloss LT. Demonstration of the mechanism by which mitral regurgitation mimics aortic stenosis. Am J Cardiol. 1978;42:1044.

59. Friedman AW, Stein L. Pitfalls in bedside diagnosis of severe acute mitral regurgitation: clinical and hemodynamic features. Chest. 1980;78:436.

60. Forrester JS, Diamond G, Freedman S, et al. Silent mitral insufﬁciency in acute myocardial infarction. Circulation. 1990;82(S5):125.

61. Raphael MJ, Steiner RE, Raftery ED. Acute mitral incompetence. Clin Radiol. 1967;18:126.

62. Grenon H, Bilodeau S. Pulmonary edema of the right upper lobe associated with acute mitral regurgitation. Can Assoc Radiol J. 1994;45:97.

63. Roach JM, Stajduhar KC, Torrington KG, et al. Right upper lobe pulmonary edema caused by acute mitral regurgitation: diagnosis by transesophageal echocardiography. Chest. 1993;103:1286.

64. Harrison MR, MacPhail B, Gurley JC, et al. Usefulness of color Doppler ﬂow imaging to distinguish ventricular septal defect from acute mitral regurgitation complicating myocardial infarction. Am J Cardiol. 1989;64:697.

65. Come PC, Riley MR, Weintraub R, et al. Echocardiographic detection of complete and partial papillary muscle rupture during acute myocardial infarction. Am J Cardiol. 1985;56:787.

66. Grayburn PA, Fehske W, Heyder O, et al. Multiplane transesophageal echocardiographic assessment of mitral regurgitation by Doppler color ﬂow mapping of the vena contracta. Am J Cardiol. 1994;74:912.

67. Kishon Y, Oh JK, Schaff HV, et al. Mitral valve operation in post-infarction rupture of a papillary muscle: immediate results and long-term follow-up of 22 patients. Mayo Clin Proc. 1992;67:1023.

68. Goodman DJ, Rossen RM, Holloway EL, et al. Effect of nitroprusside on left ventricular dynamics in mitral regurgitation. Circulation. 1974;50:1025.

69. Chaterjee K, Parmley WW, Swan HJC, et al. Beneﬁcial effects of vasodilator agents in severe mitral regurgitation due to dysfunction of subvalvular apparatus. Circulation. 1973; 48:684.

70. Gold HK, Leinbach RC, Sanders CA, et al. Intra-aortic balloon pumping for ventricular septal defect and mitral regurgitation complication myocardial infarction. Circulation. 1973;47:1191.

71. Tcheng JE, Jackman JD, Nelson CL, et al. Outcome of patients sustaining acute ischemic mitral regurgitation during myocardial infarction. Ann Intern Med. 1992;117:18.

72. Thompson CR, Buller CE, Sleeper LA, et al. Cardiogenic shock due to acute severe mitral regurgitation complicating acute myocardial infarction: a report from the SHOCK Trial Registry. J Am Coll Cardiol. 2000;36:1104.

73. Nishimura RA, Schaff HV, Shub C, et al. Papillary muscle rupture complicating acute myocardial infarction: analysis of 17 patients. Am J Cardiol. 1983;51:373.

74. Sanders RJ, Neubuerger KT, Ravin A. Rupture of papillary muscles: occurrence of rupture of the posterior muscle in posterior myocardial infarction. Dis Chest. 1957;31:316.

75. Russo A, Suri RM, Grigioni F, et al. Clinical outcome after surgical correction of mitral regurgitation due to papillary muscle rupture. Circulation. 2008;118:1528–1534.

76. Alajaji WA, Akl EA, Farha A, Jaber WA. AlJaroudi WA. Surgical versus medical management of patients with acute ischemic mitral regurgitation: a systematic review. BMC Research Notes. 2015;8:712.

77. Hammermeister K, Sethi GK, Henderson WG, et al. Outcomes 15 years after valve replacement with a mechanical versus a bioprosthetic valve: ﬁnal report of the Veterans Affairs randomized trial. J Am Coll Cardiol. 2000;36:1152–1158.

78. Mehlman DJ, Resnekov L. A guide to the radiographic identiﬁcation of prosthetic heart valves. Circulation. 1978;57:613.

79. Murphy ES. Prosthetic cardiac valves. In: Greenberg BH, Murphy ES, eds. Cardiovascular Clinics: Valvular Heart Disease. Littleton, Mass: PSG Publishing; 1987:264.

CHAPTER 26 Acute Presentations of Valvular Heart Disease 274.e3

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80. Labovitz AJ. Assessment of prosthetic heart valve function by Doppler echocardiography: a decade of experience. Circulation. 1989;80:707.

81. Kapur KW, Fan PH, Nanda NC, et al. Doppler color ﬂow mapping in the evaluation of prosthetic mitral and aortic valve function. J Am Coll Cardiol. 1989;13:1561.

82. Spain MG, Smith MD, Crayburn PA, et al. Quantitative assessment of mitral regurgitation by Doppler color ﬂow imaging: angiographic and hemodynamic correlations. J Am Coll Cardiol. 1989;13:585.

83. Alam M, Rosman HS, Hautamaki K, et al. Color ﬂow Doppler evaluation of cardiac bioprosthetic valves. Am J Cardiol. 1989;64:1389.

84. Zoghbi WA, et al. Recommendations for evaluation of prosthetic valves with echocardiography and doppler ultrasound: a report From the American Society of Echocardiography’s Guidelines and Standards Committee and the Task Force on Prosthetic Valves, developed in conjunction with the American College of Cardiology Cardiovascular Imaging Committee, Cardiac Imaging Committee of the American Heart Association, the European Association of Echocardiography, a registered branch of the European Society of Cardiology, the Japanese Society of Echocardiography and the Canadian Society of Echocardiography, endorsed by the American College of Cardiology Foundation, American Heart Association, European Association of Echocardiography, a registered branch of the European Society of Cardiology, the Japanese Society of Echocardiography, and Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2009;22(9):975–1014.

85. Currie PJ, Seward JB, Reeder GS. Continuous wave Doppler echocardiographic assessment of severity of calciﬁc aortic stenosis: a simultaneous Doppler-catheter correlative study in 100 adult patients. Ciculation. 1985;71:1162–1169.

86. Nanda NC, Coper JW, Mahan EF, et al. Echocardiographic assessment of prosthetic valves. Circulation. 1991;84(S3):I–228.

87. Bach DS. Echo/Doppler Evaluation of Hemodynamics After AVR. Principles of interrogation and evaluation of high gradiets. JACC Cardiovascular Imaging. 2010;3:294–304.

88. Nishimura A, Otto M, Bonow O, et al. 2014 AHA/ACC Guideline for the management of patients with valvular heart disease: executive summary. Circulation. 2014;129(23):2440–2492.

89. Blauwet LA, Miller FA. Echocardiographic Assessment of Prosthetic Heart Valves. Progress Cardiovasc Dis. 2014;57:100–110.

90. Dittrich HC, McCann HA, Walsh TP, et al. Transesophageal echocardiography in the evaluation of prosthetic and native aortic valves. Am J Cardiol. 1990;66:758.

91. Chaudhry FA, Herrera CJ, DeFrino PF, et al. Pathologic and angiographic correlations of transesophageal echocardiography in prosthetic heart valve dysfunction. Am Heart J. 1991;122:1057.

92. Herrera CJ, Chaudhry FA, DeFrino PF, et al. Value and limitations of transesophageal echocardiography in evaluating prosthetic or bioprosthetic valve dysfunction. Am J Cardiol. 1992;69:697.

93. Karalis DG, Chandrasekaran K, Ross JJ Jr, et al. Single-plane transesophageal echocardiography for assessing function of mechanical or bioprosthetic valves in the aortic valve position. Am J Cardiol. 1992;69:1310.

94. Alton ME, Pasierski TJ, Orsinellenni DA, et al. Comparison of transthoracic and transesophageal echocardiography in

evaluation of 47 Starr-Edwards prosthetic valves. J Am Coll Cardiol. 1992;20:1503.

95. Groundstroem K, Rittoo D, Hoffman P, et al. Additional value of biplane transesophageal imaging in assessment of mitral valve prostheses. Br Heart J. 1993;70:259.

96. Daniel WG, Mugge D, Grote J, et al. Comparison of transthoracic and transesophageal echocardiography for detection of abnormalities of prosthetic and bioprosthetic valves in the mitral and aortic positions. Am J Cardiol. 1993;71:210.

97. Habib G, Cornen A, Mesana T, et al. Diagnosis of prosthetic heart valve thrombosis: the respective value of transthoracic and transesophageal Doppler echocardiography. Eur Heart J. 1993;14:447.

98. Guerent P, Vignon P, Fournier P, et al. Transesophageal echocardiography for the diagnosis and management of non-obstructive thrombosis of mechanical mitral valve prosthesis. Circulation. 1995;91:103.

99. Mohr-Kahaly S, Kuperwasser I, Erbel R, et al. Value and limitations of transesophageal echocardiography in the evaluation of aortic prostheses. J Am Soc Echocardiogr. 1993;6:12.

100. Daniel WG, Mugge A, Martin RP, et al. Improvement in the diagnosis of abscesses associated with endocarditis by transesophageal echocardiography. N Engl J Med. 1991; 324:795.

101. Krishna Reddy N, Padmanabhan TNC, Singh S, et al. Thrombolysis in left-sided prosthetic valve occlusion: immediate and follow-up results. Ann Thorac Surg. 1994; 58:462.

102. Silber H, Khan SS, Matloff JM, et al. The St Jude valve: thrombolysis as the ﬁrst line of therapy for cardiac valve replacement. Circulation. 1993;87:30.

103. Sugano T, Fujiwara H, Adachi S, et al. Tissue-type plasminogen activator (t-PA) lysis of aortic and mitral valve thrombosis. J Cardiovasc Surg. 1993;34:259.

104. Baddour LM, Wilson WR, Bayer AS. Infective endocarditis in Adults. Circulation. 2015;132(15):1435.

105. Latib A, Naim C, De Bonis M, et al. TAVR-associated prosthetic valve infective endocarditis: results of a large, multicenter registry. J Am Coll Cardiol. 2014;64(20):2176–2178.

106. Wellford AL, Wellford LA. Prosthetic heart valves. Emerg Med Clin North Am. 1994;12:597.

107. Karthikeyan G, Senguttuvan NB, Joseph J, et al. Urgent surgery compared with ﬁbrinolytic therapy for the treatment of left-sided prosthetic heart valve thrombosis: a systematic review and meta-analysis of observational studies. Eur Heart J. 2013;34:1557–1566.

108. Lin SS, Reynertson SI, Louie EK, et al. Right ventricular volume overload results in depression of left ventricular ejection fraction: implications for the surgical management of tricuspid valve disease. Circulation. 1994;90(Pt 2):II–209.

109. Bayer AS. Infective endocarditis. Clin Infect Dis. 1993;17:313.

110. Linka A, Ritter M, Turina M, et al. Acute tricuspid papillary muscle rupture following blunt chest trauma. Am Heart J. 1992;124:799.

111. Bayezid O, Mete A, Turkay C, et al. Traumatic tricuspid insufﬁciency following blunt chest trauma. J Cardiovasc Surg. 1993;34:69.

112. Silverman BD, Carabajal NR, Chorches MA, et al. Tricuspid regurgitation and acute myocardial infarction. Arch Intern Med. 1982;142:1394.

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113. Vatterott PJ, Nishimura RA, Gersh BJ, et al. Severe isolated tricuspid insufﬁciency in coronary artery disease. Int J Cardiol. 1987;14:295.

114. Braverman AC, Coplen SE, Mudge GH, et al. Ruptured chordae tendineae of the tricuspid valve as a complication of endomyocardial biopsy in heart transplant patients. Am J Cardiol. 1990;66:111.

115. Crumbley AJ III, Van Bakel AB. Tricuspid valve repair for biopsy-induced regurgitation after cardiac transplantation. Ann Thorac Surg. 1994;58:1156.

116. Tucker PA II, Jin BS, Gaos CM, et al. Flail tricuspid leaﬂet after multiple biopsies following orthotopic heart transplantation: echocardiographic and hemodynamic correlation. J Heart Lung Transplant. 1994;13:466.

117. Huddleston CB, Rosenbloom M, Goldstein JA, et al. Biopsyinduced tricuspid regurgitation after cardiac transplantation. Ann Thorac Surg. 1994;57:832.

118. Suzuki Y, Kambara H, Kadota K, et al. Detection and evaluation of tricuspid regurgitation using a real-time, two-dimensional, color-coded Doppler ﬂow imaging system: comparison with two-dimensional echocardiography and right ventriculography. Am J Cardiol. 1986;57:811.

119. Skaerpe T, Hatle L. Noninvasive estimation of systolic pressure in the right ventricle in patients with tricuspid regurgitation. Eur Heart J. 1986;7:704.

120. San Román JA, Vilacosta I, Zamorano JL, et al. Transesophageal echocardiography in right-sided endocarditis. J Am Coll Cardiol. 1993;21:1226.

121. Zehender M, Kasper W, Kander E, et al. Right ventricular infarction as an independent predictor of prognosis after acute myocardial infarction. N Engl J Med. 1993;328:981.

122. Stern HJ, Sisto DA, Strom JA, et al. Immediate tricuspid valve replacement for endocarditis: indications and results. J Thorac Cardiovasc Surg. 1986;91:163.

123. Arbulu A, Holmes RJ, Asfaw I. Tricuspid valvulectomy without replacement: twenty years experience. J Thorac Cardiovasc Surg. 1991;102:917.

124. Allen MD, Slachman F, Eddy CA, et al. Tricuspid valve repair for tricuspid valve endocarditis: tricuspid valve “recycling. Ann Thorac Surg. 1991;51:593.

125. Jagger JD, McCaughan BC, Pawsey CGK. Tricuspid valve endocarditis cured by excision of a single vegetation. Am Heart J. 1986;112:626.

OUTLINE

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Deﬁnition, 275 Incidence and Prevalence, 275 Pathophysiology, 275 Evaluation and Management, 276 Prognosis, 279 Speciﬁc Hypertensive Emergencies, 281

Cardiovascular Emergencies, 281

Acute Coronary Syndrome, 281 Aortic Dissection, 281 Acute Pulmonary Edema, 281

Neurologic Emergencies, 281

Hypertensive Encephalopathy/Posterior Reversible

Encephalopathy Syndrome, 281

Hypertensive Emergencies

Brigitte M. Baumann, Richard M. Pescatore II

Subarachnoid Hemorrhage, 286 Intracerebral Hemorrhage, 287 Ischemic Cerebrovascular Accident, 287

Acute Renal Insufﬁciency, 288 Preeclampsia or Eclampsia, 288

Perioperative Hypertension, 289

Hyperadrenergic States, 290

Sympathomimetic Agents, 290 Abrupt Cessation of Antihypertensive Drugs, 290 Pheochromocytoma and Paraganglioma, 291 Autonomic Dysfunction, 291

DEFINITION

Hypertensive emergencies are characterized by severe elevations in blood pressure (BP) (>180/120 mm Hg) complicated by impending or progressive target organ dysfunction.1 Targeted organs typically include the aorta, brain, eyes, heart, and kidneys. Immediate (minutes to hours) BP reduction is essential to prevent further morbidity. This contrasts with hypertensive urgencies, in which severe elevations in BP are not accompanied by target organ dysfunction. In these cases, BP reduction may occur in an outpatient setting with oral medication over 24 to 48 hours. The terms malignant hypertension and accelerated hypertension are older, less commonly used, and have been replaced by these newer terms in national guidelines. Collectively, hypertensive emergencies and urgencies are referred to as hypertensive crises.

Table 27.1 outlines deﬁnitions and management goals of hyper-

tensive emergencies.

1-6

INCIDENCE AND PREVALENCE

Approximately 1 billion individuals have hypertension worldwide; by 2025, 1.6 billion will be affected.7 The prevalence in developing countries is rapidly increasing, with 16% of the adult population in sub-Saharan Africa and 27% in mainland China categorized as hypertensive. Mass migrations from rural to urban settings and changes in lifestyle and diet are considered major contributing

8,9

factors.

In the United States, the prevalence has also increased

from 24% to 29% from the 1990s to 2008.10 In France, Germany, Italy, Spain, and the United Kingdom, the total population is projected to grow by only 6% from 2010 to 2025 but the prevalence of hypertension is anticipated to increase by 15%. This increase is due primarily to aging of the populations.

Although worldwide prevalence of hypertension is increasing, the proportion of patients who will experience a hypertensive emergency remains quite low. Of emergency department (ED) patients, 1% to 6% will present with severe hypertension (>180/120 mm Hg); of those, between one-third to one-half will have target organ damage. this risk at 2 per 1000 ED visits.

Risk factors for development of hypertensive emergency include male sex, older age, greater mean diastolic BP (DBP),

and medication nonadherence. multifactorial: lack of health insurance or primary care physician, insufﬁcient funds to pay for medications, and treatment ambivalence (lower hypertension knowledge, medication side effects and feeling that the medications do not help) may all play a

role.

12–16

A more recent estimate places

13,15,18

Nonadherence is likely

PATHOPHYSIOLOGY

Although the pathophysiology of hypertensive emergencies is incompletely understood, an initial abrupt rise in vascular resistance appears to be an initiating step. disruption or deactivation of the arterial baroreﬂex, BP continues

20,21

When accompanied by

275

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