Acute aortic regurgitation caused by non-bacterial thrombotic endocarditis

Kardaras, Fotios; Kardara, Dimitra; Rontogiani, Dimitra P.; Sioras, Elias; Christopoulou-Cokkinou, V.; Lolas, Christos; Anthopoulos, L.

doi:10.1093/oxfordjournals.eurheartj.a061062

Cited by 8 publications

(4 citation statements)

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“…16 -18 Other less common causes of acute AR include nonbacterial endocarditis, 19 laceration of the aorta, 20 and complications of invasive procedures such as aortic valvuloplasty and percutaneous balloon dilatation of aortic coarctation. 21 Fortunately, acute AR, which has a poor prognosis, is rare.…”

Section: Etiologymentioning

confidence: 99%

Valvular Heart Disease

2005

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Abstract-Aortic regurgitation (AR) is characterized by diastolic reflux of blood from the aorta into the left ventricle (LV).Acute AR typically causes severe pulmonary edema and hypotension and is a surgical emergency. Chronic severe AR causes combined LV volume and pressure overload. It is accompanied by systolic hypertension and wide pulse pressure, which account for peripheral physical findings, such as bounding pulses. The afterload excess caused by systolic hypertension leads to progressive LV dilation and systolic dysfunction. The most important diagnostic test for AR is echocardiography. It provides the ability to determine the cause of AR and to assess the severity of AR and its effect on LV size, function, and hemodynamics. Many patients with chronic severe AR may remain clinically compensated for years with normal LV function and no symptoms. These patients do not require surgery but can be followed carefully for the onset of symptoms or LV dilation/dysfunction. Surgery should be considered before the LV ejection fraction falls below 55% or the LV end-diastolic dimension reaches 55 mm. Symptomatic patients should undergo surgery unless there are excessive comorbidities or other contraindications. The primary role of medical therapy with vasodilators is to delay the need for surgery in asymptomatic patients with normal LV function or to treat patients in whom surgery is not an option. The goal of vasodilator therapy is to achieve a significant decrease in systolic arterial pressure. Future therapies may focus on molecular mechanisms to prevent adverse LV remodeling and fibrosis. Key Words: aorta Ⅲ echocardiography Ⅲ valves Ⅲ ventricles A ortic regurgitation (AR) is characterized by diastolic reflux of blood from the aorta into the left ventricle (LV) due to malcoaptation of the aortic cusps. Its clinical presentation is variable and depends on a complex interplay of a number of factors, including acuity of onset, aortic and LV compliance, hemodynamic conditions, and severity of the lesion. Although chronic AR is generally well tolerated for many years, acute AR may lead to rapid cardiac decompensation and, if untreated, to early death. 1 This review focuses on the clinical manifestations of AR, evaluation of its severity and hemodynamic consequences, and its treatment. PrevalenceThe prevalence of chronic AR and incidence of acute AR are not precisely known. Singh et al 2 reported the prevalence of chronic AR detected by color Doppler echocardiography in a large unselected adult population (the Framingham Offspring Study). The overall prevalence AR in men was 13% and in women 8.5%. However, most of the AR in this population was trace or mild in severity; moderate or severe AR was rare (Table 1). Multiple logistic regression analysis revealed age and male gender to be predictors of AR. Interestingly, hypertension did not predict AR on multivariate analysis, confirming results of earlier studies that hypertension is associated with modest increases in aortic root size but not AR when age is included in the...

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Section: Etiologymentioning

confidence: 99%

Valvular Heart Disease

2005

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“…We have reported a case of non-bacterial thrombotic endocarditis (NBTE) [4][5][6][7][8][9][10] occurring as a rare complication of PTMC despite adequate anticoagulation therapy. The protrusion recognized in this case appeared to be an organized thrombus, based on its echocardiographic and microscopic features.…”

Section: Discussionmentioning

confidence: 99%

“…2,3) Furthermore, an indication of PTMC has been extended to include even relatively complicated cases. To date, there have been no reports of the occurrence of non-bacterial thrombotic endocarditis (NBTE) [4][5][6][7][8][9][10] at the dilated site after this procedure. We report a case of thrombus formation that occurred insidiously as a rare complication of PTMC.…”

Section: Percutaneous Transvenous Mitral Commissurotomy (Ptmc) Is Now Anmentioning

confidence: 99%

“…14,15) On the other hand, NBTE also develops in patients with chronic rheumatic valvulitis 10) , or non-specific abnormalities such as fibrous thickening or fibrous and hyaline nodularitis of heart valves. Mechanical damage to valves may occur with catheters used for venous pressure 4) or pulmonary artery pressure monitoring 8) , leading to the formation of verrucae.…”

Section: )mentioning

confidence: 99%

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Development of Non-bacterial Thrombotic Endocarditis after Percutaneous Transvenous Mitral Commissurotomy for Severely Calcified Mitral Stenosis.

Tomimoto

Shigenori²,

Suzuki³

et al. 2000

Jpn Heart J

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SUMMARYWe encountered a case of mitral stenosis, complicated with non-bacterial thrombotic endocarditis, that developed after percutaneous transvenous mitral commissurotomy (PTMC). A 71-year-old female Japanese patient had severe congestive heart failure and underwent PTMC for critical and severely calcified mitral stenosis. Four weeks later, the echocardiogram demonstrated a highly echoic protrusion in the postero-medial commissure of the mitral valve. There was little evidence of inflammation at that time. She had been anticoagulated adequately since she was admitted. The patient underwent replacement of the mitral valve. She did not show any evidence of systemic embolization. Microscopic evaluation showed only organized thrombus but no evidence of inflammation in the mitral valve. Silent development of non-bacterial thrombotic endocarditis after PTMC should be recognized as a rare but potentially lethal complication of PTMC. ( 1-3) With increasing performance of PTMC, the therapeutic effectiveness of this procedure has come to be widely accepted despite its risk.2, 3) Furthermore, an indication of PTMC has been extended to include even relatively complicated cases. To date, there have been no reports of the occurrence of non-bacterial thrombotic endocarditis (NBTE) [4][5][6][7][8][9][10] at the dilated site after this procedure. We report a case of thrombus formation that occurred insidiously as a rare complication of PTMC.

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