Native and Prosthetic Valve Emergencies

Abstract

Native valvular emergencies are nearly always regurgitant in nature, whereas acute prosthetic valve dysfunction can be either regurgitant or stenotic. Regardless of the etiology, the presentation of acute valvular pathology differs significantly from chronic disease in both clinical presentation and in its appearance on diagnostic modalities, and appropriate recognition is critical to the choice of the appropriate therapeutic modality. Intrinsic to the recognition of a valvular emergency is a knowledge of those conditions for which a high index of suspicion must be maintained. This article addresses the etiologies, presentation, and diagnosis of these conditions and presents the relevant data that bears on which therapy may be most appropriate for which condition.

Acute heart failure and valvular heart disease: A scientific statement of the Heart Failure Association, the Association for Acute CardioVascular Care and the European Association of Percutaneous Cardiovascular Interventions of the European Society of Cardiology

“…61,62 LV hypertrophy is a key adaptive mechanism to the pressure load but it increases LV mass leading to discrepancy in oxygen demand and supply and relative myocardial ischaemia. [11][12][13][14][15][16] Afterload mismatch is initially responsible of decreasing in EF and stroke volume, but later on long-term exposure to pressure overload and demand ischaemia produce intrinsic myocardial contractility dysfunction with further decrease of EF, LV dilatation and secondary mitral regurgitation [11][12][13] • Various precipitants may intervene in different stages of severity and ventricular adaptation and may lead to decompensation, when SV is decreased at rest, and development of AHF [11][12][13][14][15][16] • Acute obstruction of aortic prosthetic valve may lead to AHF. The acute outflow obstruction, if left untreated, leads to a rapid clinical deterioration with decrease of SV and LV dilatation [11][12][13][14][15][16] • May present with any clinical profile • CS presentation is strongly related to mortality even after interventions 121,123 • RHF may occur in the later stages of AS evolution as consequence of PH or associated right-sided VHD 37 Severe AR • Haemolytic anaemia is the consequence of paravalvular leak 15,16,157 • RHF may occur as a consequence of PH or associated right-sided VHD • In 25% of patients, systolic dysfunction is also present due to chronic decrease of preload but also due to rheumatic cardiomyopathy [11][12][13][14][15][16] • Acute obstruction of mitral prosthetic valve may lead to AHF.…”

“…The acute outflow obstruction, if left untreated, leads to a rapid clinical deterioration with decrease of SV and LV dilatation [11][12][13][14][15][16] • May present with any clinical profile • CS presentation is strongly related to mortality even after interventions 121,123 • RHF may occur in the later stages of AS evolution as consequence of PH or associated right-sided VHD 37 Severe AR • Haemolytic anaemia is the consequence of paravalvular leak 15,16,157 • RHF may occur as a consequence of PH or associated right-sided VHD • In 25% of patients, systolic dysfunction is also present due to chronic decrease of preload but also due to rheumatic cardiomyopathy [11][12][13][14][15][16] • Acute obstruction of mitral prosthetic valve may lead to AHF. The acute obstruction leads to a rapid clinical deterioration [11][12][13] • Resting symptoms usually develop when the valve area is <1.0 cm 2 . However, symptoms often occur in patients with larger valve areas if the time of diastolic filling decreases and/or transmitral flow increases (pregnancy, infection, new-onset or rapid AF, fever, anaemia, hyperthyroidism or haemodynamic shifts in the perioperative period of patients undergoing non-cardiac surgery).…”

“…Assessing aetiology may not be immediately available in critically ill patient and accurate valvular assessment can be challenging with multiple VHD or in those with extreme loading conditions. [11][12][13][14] There are no rigorously conducted randomized controlled trials in the setting of VHD with AHF. Besides, patients with severe VHD are often excluded from AHF randomized controlled trials and this leads to lack of a clear-cut strategy.…”

Structural Heart Disease Emergencies

“…Infective endocarditis and valve thrombosis are major causes of acutely worsened valvular function, along with progressive chronic degeneration of a native or prosthetic valve. 9 Mechanical complications of AMI, including acute ischemic MR and VSD, represent well-characterized SHD emergencies. 10 Right ventricular failure is a common consequence of left-sided SHD lesions due to development of secondary pulmonary hypertension, especially for acutely decompensated chronic lesions.…”

“…57 While acute MR can occur due to worsening of chronic MR leading to decompensation from volume overload with LV dilation, de novo severe MR typically results from infective endocarditis, chordal rupture with a flail segment or leaflet, or papillary muscle rupture after AMI. 9 Mitral regurgitation can be highly dynamic and influenced by loading conditions and contractility, making the evaluation of MR severity in acutely ill patients challenging. 58 It is often necessary to re-evaluate MR severity once volume overload and systemic hypertension are adequately controlled, particularly for functional MR in the absence of major valve pathology (Table 2).…”