Worldwide, the leading cause of aortic insufficiency is rheumatic disease. However, in Western Europe and North America, the leading cause of AI is either congenital or degenerative disease. The incidence increases with age and is more common in men than women.8 Per the Framingham study, the prevalence of AI in the western world was reported to be 4.9%, with regurgitation of moderate or greater severity occurring at approximately 0.5%.9 Severe AI is known to have increased morbidity and mortality compared to the general population and with conservative management, the majority of patients will develop heart failure in ten years.10
The causes of acute AI differ from chronic AI in etiology and presentation. In chronic AI, the left ventricle dilates and remodels to maintain forward stroke volume, cardiac output, and left ventricle end-diastolic pressure (LVEDP). In contrast, remodeling does not occur in acute regurgitation. The normal ventricular size and a marked increase in LVEDP lead to impaired forward stroke volume, decreased systolic pressure, and narrow pulse pressure.11–12 The events that ensue are ineffective forward stroke volume, compensatory tachycardia, hypotension, end-organ failure, and other evidence of cardiogenic shock.13
In this case report, we are uncertain as to the exact etiology of her acute AI. The possible mechanisms are either BCI or an acute hypertensive event given her prior illicit drug use. BCI occurs from several mechanisms: the direct insult to the chest such as steering wheel trauma leading to compression of the heart against the vertebral column, acceleration-deceleration impact leading to a torsion at the fixation sites such as the pulmonary trunk, hydraulic effect transmitting the increased intra-abdominal pressure to the right atrium via the draining inferior vena cava (IVC) or a blast injury.6,14−16 The mechanism for the BCI in this patient is presumably a motor vehicle accident resulting in sternal fracture and direct chest trauma. This trauma causes a sudden increase in intrathoracic pressure during diastole, when the pressure gradient across the aortic valve is maximal and the valve is closed, resulting in an aortic valve rupture.17
In contrast, there have been a few case reports describing aortic rupture from a hypertensive episode. Ayogi et al described two cases of severe aortic regurgitation due to non-traumatic rupture of the aortic valve commissures. Both patients underwent aortic valve replacement successfully.18 Our patient is prone to hypertensive episodes as a side effect of her methamphetamines and cocaine use. However, there has been no reported case reports of either illicit drugs directly causing a valve rupture without the presence of an associated aortic dissection.
Regardless of the mechanism, prompt diagnosis, stabilization, and treatment are imperative because of rapid deterioration and heart failure secondary to acute aortic regurgitation.19 Medical management is directed towards reducing pulmonary venous congestion and optimizing cardiac output in an attempt to stabilize the hemodynamics before surgery. Invasive monitoring such as a Pulmonary artery catheter is also useful for monitoring hemodynamics and directing medical therapy. Echocardiography is the noninvasive test of choice. If the patient is stable, TEE achieves better visualization of the valvular anatomy and myocardial function.20 Cardiac catheterization remains the gold standard for providing information concerning aortic insufficiency including abnormalities associated with the aortic root and coronary vessels in stable patients. Ultimately when there is hemodynamic instability, timely surgical intervention is warranted in an urgent fashion.1This case represents an acute aortic insufficiency from unknown etiology. Our patient was identified early and treated expeditiously with an excellent outcome.