VALVULAR DISEASE ACCSAP Flashcards
Vasodilator therapy in chronic severe primary MR?
Vasodilator therapy is not indicated for normotensive asymptomatic patients with chronic primary MR and normal left ventricular (LV) systolic function.
Because vasodilator therapy appears to be effective in acute severe symptomatic MR, it seems reasonable to attempt afterload reduction in chronic asymptomatic MR with normal LV function in an effort to forestall the need for surgery. However, the results from the limited number of trials addressing this therapy have been disappointing, demonstrating little or no clinically important benefit.
Conversely, because vasodilators decrease LV size and mitral closing force, they may increase MVP, worsening rather than decreasing the severity of MR. The foregoing does not apply to patients with concomitant hypertension. Hypertension must be treated because of the well known morbidity and mortality associated with that condition and because increased LV systolic pressure by itself increases the systolic transmitral gradient and worsens the severity of MR.
Exercise stress testing in aortic stenosis?
Exercise stress testing is reasonable to assess physiological changes with exercise and to confirm the absence of symptoms in reportedly asymptomatic patients with a calcified aortic valve and an aortic velocity ≥4.0 m/sec or a mean pressure gradient of ≥40 mm Hg (stage C)
Choice of bioprosthetic versus mechanical valve replacement?
The choice of which type of valve, bioprosthetic versus mechanical, is an individual one and should be done with shared decision-making based on the individual’s preferences, risks of long-term anticoagulation, and contraindications to anticoagulation.
A bioprosthesis is recommended in patients of any age for whom anticoagulant therapy is contraindicated, cannot be managed appropriately, or is not desired.
Factors that favor mechanical prosthesis include age <50, low risk for anticoagulation complications, adherence to medical therapy, additional reasons for long term anticoagulation, small risk for re-intervention and small aortic root size.
While the risk for reoperation with bioprosthetic valves is greater in younger patients, this must be balanced against the risk of bleeding such as in a patient who is an avid motorcyclist.
Bileaflet mechanical AVR interruption of anticoagulation?
Temporary interruption of vitamin K antagonist (VKA) anticoagulation, without bridging agents while the international normalized ratio (INR) is subtherapeutic, is recommended in patients with a bileaflet mechanical AVR and no other risk factors for thrombosis who are undergoing invasive or surgical procedures.
When interruption of oral VKA therapy is deemed necessary, the agent is usually stopped 3-4 days before the procedure
Bridging therapy in patients with mechanical valves when VKA held prior to surgery?
“Bridging” therapy with either intravenous unfractionated heparin or low-molecular-weight heparin has evolved empirically to reduce thromboembolic events during temporary interruption of oral anticoagulation in higher-risk patients, such as those with a mechanical mitral valve replacement or AVR and additional risk factors for thromboembolism (e.g., atrial fibrillation, previous thromboembolism, hypercoagulable condition, older-generation mechanical valves [ball-cage or tilting disc], left ventricular systolic dysfunction, or >1 mechanical valve).
Treatment for primary assymptomatic severe primary MR?
Patient with asymptomatic primary severe MR (stage C1) with a normal EF and normal LV dimensions with a surgical risk of <1% and and a high likelihood of successful MV repair (>95%) may be considered for surgical MV repair to prevent long-term sequela and adverse remodeling (Class IIa). MV repair by an experienced surgeon is preferred over replacement. There is no indication for transcather repair as the patient is at a low risk for surgery. If observation is chosen, a repeat echocardiogram should be obtained in 6-12 months for severe MR.
Primary TR causes?
Primary disorders causing TR include rheumatic heart disease, prolapse, congenital disease (Ebstein’s), infective endocarditis, radiation, carcinoid syndrome, blunt chest wall trauma, RV endomyocardial biopsy-related trauma, and intra-annular RV pacemaker or implantable cardioverter defibrillator leads.
Rheumatic tricuspid valve disease typically includes diffuse leaflet thickening with restriction of opening due to commissural fusion, chordal shortening, and calcification with characteristic diastolic doming. In carcinoid syndrome, liver metastases produce 5-hydroxyindoleacetic acid which causes a unique echocardiographic appearance of the RV including leaflets that are short, thick, and with systolic and diastolic restriction.
Secondary tricuspid regurgitation?
Approximately 80% of cases of significant TR are functional in nature and related to tricuspid annular dilation and leaflet tethering in the setting of RV remodeling due to pressure and/or volume overload.
Pacemaker leads and TR?
Severe TR can be caused by restriction from pacemaker lead. Endocardial leads can impair the structure and function of the tricuspid valve. Injury can also occur during implantation or extraction. Chronic interaction between the endocardial leads and tricuspid valve leaflets and/or chords can result in inflammation and fibrosis leading to entrapment of the lead. The resulting TR will typically exhibit eccentric rather than a central trajectory, with the septal leaflet being the most common leaflet to be entrapped.
Note: We would see elevated RA pressure, v-waves without pulmonary hypertension
Treatment of assymptomatic primary MR stage C2?
Mitral valve (MV) surgery is recommended for asymptomatic patients with chronic severe primary MR and left ventricular (LV) dysfunction (LVEF of 30-60% and/or LVESD of 40 mm, stage C2).
Ideally, MV surgery should be performed when the patient’s LV approaches, but has not yet reached the parameters that indicate systolic dysfunction (LVEF of 60% or LVESD of 40 mm). Because symptoms do not always coincide with LV dysfunction, imaging surveillance is used to plan surgery before severe dysfunction has occurred. If moderate LV dysfunction is already present, prognosis is reduced following MV operation. Thus, further delay (even though symptoms are absent) will lead to greater LV dysfunction and a still worse prognosis. Because the loading conditions in MR allow continued late ejection into a lower-impedance left atrium, a higher cutoff for “normal” LVEF is used in MR than in other types of heart disease. Although it is clearly inadvisable to allow patients’ LV function to deteriorate beyond the benchmarks of an LVEF of 60% and/or LVESD of 40 mm, some recovery of LV function can still occur even if these thresholds have been crossed.
MV repair is recommended in preference to MV replacement when surgical treatment is indicated for patients with chronic severe primary MR involving the anterior leaflet or both leaflets when a successful and durable repair can be accomplished, thus MV repair is the preferred choice in this patient.
Transcathetar mitral valve repair?
Transcatheter MV repair may be considered for severely symptomatic patients (New York Heart Association [NYHA] class III-IV) with chronic severe primary MR (stage D) who have favorable anatomy for the repair procedure and a reasonable life expectancy, but who have a prohibitive surgical risk because of severe comorbidities and remain severely symptomatic despite optimal guideline directed medical therapy (GDMT) for heart failure (HF; Level of Evidence B). A randomized controlled trial of percutaneous MV repair using the MitraClip device versus surgical MV repair was conducted in the United States. The clip was found to be safe, but less effective than surgical repair because residual MR was more prevalent in the percutaneous group. However, the clip reduced the severity of MR, improved symptoms, and led to reverse LV remodeling. Percutaneous MV repair should only be considered for patients with chronic primary MR who remain severely symptomatic with NYHA class III-IV HF symptoms despite optimal GDMT for HF and who are considered inoperable.
Ejection clicks?
Ejection clicks are high-pitched sounds that occur at the moment of maximal opening of the aortic or pulmonary valves. They are heard just after the first heart sound. The sounds occur in the presence of a dilated aorta or pulmonary artery or in the presence of a bicuspid or flexible stenotic aortic or pulmonary valve
Pulmonic ejection click/sound?
The most helpful distinguishing feature of a pulmonary ejection sound is its decreased intensity, or even its disappearance during the inspiratory phase of respiration. During expiration, the valve opens rapidly from its fully closed position; sudden “halting” of this rapid opening movement is associated with a maximal intensity of the ejection sound. With inspiration, the increased venous return to the right ventricle (RV) augments the effect of right atrial systole and causes partial opening of the pulmonary valve prior to ventricular systole. The lack of a sharp opening movement of the pulmonary valve explains the decreased intensity of the pulmonary ejection sound during inspiration. Thus, the best way to confirm that the patient has pulmonic stenosis is to assess the intensity of the murmur on inspiration.
Note: If ejection click and murmur are heard only at the left sternal border is consistent with pulmonic rather than aortic stenosis. The only right-sided auscultatory event that diminishes with inspiration is the pulmonary ejection click associated with pulmonary valve stenosis.
Hand grip?
Sustained hand grip for 20-30 seconds leads to an increase in systemic vascular resistance, arterial pressure, cardiac output, and left ventricular (LV) volume and filling pressure. Hand grip is most useful in differentiating between the ejection systolic murmur of aortic stenosis and the regurgitant murmur of mitral regurgitation (MR). Intensity of the murmur of aortic stenosis tends to decrease along with a decreased transvalvular pressure gradient, while the severity and murmur of MR increase.
Valsalva manuever?
During the straining phase, phase 2, of Valsalva there is a decrease in venous return, RV and LV volumes, stroke volumes, mean arterial pressure, and pulse pressure; this is associated with a reflex increase in heart rate. The murmur of hypertrophic cardiomyopathy (HCM) increases in intensity as the LV outflow size decreases with a decreased venous return. In mitral valve prolapse (MVP) there is an early onset of the click and murmur due to the decrease in LV volume.
Squatting?
Squatting from a standing position is associated with a simultaneous increase in venous return (preload) and systemic vascular resistance (afterload) and a rise in arterial pressure. In HCM, intensity of the ejection systolic murmur declines because of an increased LV volume and arterial pressure, which increase the effective orifice size of the outflow tract. In patients with MVP there is a delay in the onset of the click and a shortening of the late systolic murmur. These changes reflect the delay in prolapse induced by the increase in preload. However, as MR becomes more severe, the murmur may increase in intensity with squatting because of the increase in afterload.
Non holosystolic MR estimation?
Parameters which are measured in a single frame like PISA, vena contracta width (VCW), or jet area can lead to significant overestimation of the severity of MR, especially in the setting of late systolic MR. The presence of normal LV and LA size should raise the possibility of overestimation by quantitative measure in this asymptomatic patient.
When calculated using the data from the echocardiogram, the instaneous effective regurgitant orifice area (EROA) is 0.5 cm2, which is consistent with severe MR (see calculations below). However, the calculated regurgitant volume is in the mild range. This is most likely secondary to late systolic MR as opposed to holosystolic MR. This is commonly seen in mitral prolapse where there is late systolic regurgitation yielding a small regurgitant volume. MR duration is a common reason for discrepancy between the calculated EROA and regurgitant volume.
Note: The MR jet would be expected to be anteriorly directed in this patient with posterior leaflet prolapse.
Regurgitant volume from PISA?
Flow = [(2) x (3.14) x (PISA r2) x (Aliasing velocity)]
EROA = [(2) x (3.14) x (PISA r2) x (Aliasing velocity)]/Vmax MR jet
Regurgitant volume is then calculated according the formula:
regurgitant volume = EROA x VTI of MR jet
Secondary prophylaxis for rheumatic fever?
Prophylaxis choices for RF include penicillin V twice daily, monthly benzathine penicillin G intramuscular injection, or daily sulfadiazine.
For those patients with residual valvular disease, the recommended duration is to continue penicillin prophylaxis for 10 years from the last episode of acute rheumatic fever or until 40 years of age (whicever is longer). If there was acute carditis but no residual valve disease, the recommendation is for 10 years or until 21 years of age (whichever is longer). If there was rheumatic fever without carditis, the recommendation is for 5 years or until 21 years of age (whichever is longer).
Endocarditis prophylaxis?
Antibiotic prophylaxis against endocarditis is indicated for those patients undergoing dental procedures involving manipulation of gingival tissues who are at highest risk of complications. These high-risk patients include those with a prosthetic cardiac valve or prosthetic valve repair material, a prior history of infective endocarditis, cardiac transplant with valvulopathy, completely repaired congenital heart disease (CHD) with percutaneous or surgical repair occurring within the previous 6 months, repaired CHD with residual shunts or defects that impair endothelialization of prosthetic material, and unrepaired cyanotic CHD.
Antibiotic prophylaxis is required in these patients who are undergoing dental procedures that involve manipulation of the gingival tissues, the periapical region of the teeth, or perforation of oral mucosa. There are no prospective studies to suggest benefit from antibiotic prophylaxis in nondental procedures.
Prosthetic valve stenosis?
Transthoracic echocardiography is the first-line test for diagnosing prosthetic valve dysfunction such as stenosis which can occur in the setting of sporadic medical care, suspicious for valve thrombosis from inadequate anticoagulation.
Expected findings would be an elevated transvalvular velocity and gradient; a prolonged (>100 msec) acceleration time; a reduced effective orifice area (<1 cm2); and a reduced dimensionless index (<0.3).
Severe aortic stenosis management?
The recommendation for either surgical aortic valve replacement (AVR) or transcather AVR among patients aged 65 to 80 years old with severe, symptomatic AS (stage D), after consideration by a heart valve team, is a Class I (LOE A) in the 2020 guideline for patients with valvular heart disease.
Balloon aortic valvuloplasty for severe AS?
Percutaneous aortic balloon dilation has an important role in treating children, adolescents, and young adults with AS, but its role in treating older patients is very limited. The mechanism by which balloon dilation modestly reduces the severity of stenosis in older patients is by fracturing calcific deposits within the valve leaflets and, to a minor degree, stretching the annulus and separating the calcified or fused commissures. Immediate hemodynamic results include a 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 aortic regurgitation, restenosis, and clinical deterioration, occur within 6-12 months in most patients. Therefore, in patients with AS, percutaneous aortic balloon dilation is not a substitute for AVR.
Anticoagulation for mechanical valve prosthesis?
Effective oral antithrombotic therapy in patients with mechanical heart valves requires continuous vitamin K antagonist (VKA) anticoagulation with an international normalized ratio (INR) in the target range. It is preferable to specify a single INR target for each patient and to recognize that the acceptable range includes 0.5 INR units on each side of this target.
Direct oral anticoagulants are not recommended in patients with mechanical valves. The one randomized controlled trial of dabigatran compared with warfarin in patients with mechanical valves was stopped early due to higher rates of bleeding and thrombosis in the dabigatran arm. No other direct oral anticoagulants have been studied in this patient population
Note: In contrast to prior guidelines, the 2020 American College of Cardiology/American Heart Association (ACC/AHA) Guideline for the Management of Patients With Valvular Heart Disease no longer recommends routine low-dose aspirin use for patients with mechanical prosthetic heart valves
S.Bovis endocarditis?
Colon cancer screening is mandatory if the pathogen is Streptococcus (S.) bovis. The association between colonic carcinoma and endocarditis was reported as early as 1951, but it was only in 1977 that S. gallolyticus (previously S. bovis) was recognized by Klein et al. as the pathogen agent specifically related to the presence of a colonic cancer
Echocardiography follow up after valve prosthesis?
Current guidelines recommend a baseline postprocedural study (TTE) ideally performed 1 to 3 months after intervention to ensure loading conditions have returned to normal. An echocardiographic examination performed 6 weeks to 3 months after valve implantation is essential to establish a baseline for comparison should complications or deterioration occur later (Class I recommendation, Level of Evidence B).
Severe acute vs chronic aortic regurgitation?
In severe acute AR echocardiography reveals preclosure of the MV due to the rapidly rising left ventricular diastolic pressure as a result of his severe AR. This also results in the soft S1 observed. As opposed to chronic AR, the difference between the aortic and left ventricular pressures in diastole may be small in acute AR and there may be little diastolic murmur. Likewise the pulse pressure may not be wide, and there may be none of the classic hemodynamic findings of chronic AR.
Mitral valve findings in severe acute AR?
Early closure of the MV (normally should be right after or on QRS)
Fluttering on the anterior MV leaflet
Prosthetic valve thrombosis?
Patients presenting with a thrombosed left-sided mechanical prosthetic valve who have symptoms should be treated promptly. It is a Class Ib-NR recommendation to treat patients urgently with a slow infusion of a low-dose fibrinolytic therapy or emergent cardiac surgery. The decision to pursue fibrinolysis should be determined based on clinical factors using a multidisciplinary heart team approach and a shared decision-making process with the patient.
If a patient has no prior history of valve thrombosis, mild symptoms, a small thrombus burden, and a low bleeding risk, it is reasonable to consider fibrinolytic therapy before considering emergent surgery. The success rate of fibrinolysis is >90% with bleeding and embolic rates <2%. IV heparin alone would not be used to treat valve thrombosis but likely would be used to bridge this patient upon reinitiating warfarin. There is no indication of infective endocarditis, so empiric vancomycin is not appropriate. Transcatheter aortic valve replacement cannot be performed in a mechanical valve and is not indicated for treatment of prosthetic valve thrombosis
Percutaneous balloon mitral commissurotomy (PBMC) for MS?
Transesophageal echocardiography should be performed in patients planning percutaneous balloon mitral commissurotomy (PBMC) to assess for the presence and degree of MR and to rule out left atrial or left atrial appendage thrombus prior to the procedure (Class I). PBMC is indicated in symptomatic patients with severe MS (Class I) and in asymptomatic patients with new onset AF and favorable valve morphology (Class IIB) (Figure 1).
Antibiotic regimens for infective endocarditis?
