Infective endocarditis (IE) is a life-threatening infection characterized by inflammation of the endocardial surface, most commonly involving the cardiac valves. It typically presents with fever and a new or changing heart murmur, while severe complications include embolic events, valvular destruction, and heart failure. IE is also associated with peri-annular extension, systemic embolization, and, rarely, acute aortic dissection (AD) [¹,²]. The coexistence of IE and AD is exceptionally uncommon, with the literature limited primarily to isolated case reports in both adult and pediatric populations; robust incidence estimates are lacking [³,⁴]. There are no published case reports of infective endocarditis (IE) involving a tricuspid aortic valve concurrently with Stanford type A aortic dissection. We report a case of IE with severe aortic regurgitation (AR) complicated by Type A AD in a tricuspid aortic valve, highlighting an atypical presentation without chest pain and underscoring the importance of high clinical suspicion and early imaging [¹].

A 40-year-old male, with no known comorbidities, non-significant cardiac family history, and no reported connective tissue disorders, presented to the emergency department with a complaint of intermittent low-grade fevers for the past 4 months and shortness of breath for 5 days. The fevers were not associated with sore throat, chest pain, or palpitations. The rest of the systematic review was unremarkable.

On examination, visible neck pulsations were noted. Blood pressure was 90/60 mmHg in the right arm and 110/70 mmHg in the left arm. The pulse rate was 110 bpm, high volume, and the patient was afebrile. Cardiovascular examination revealed a diastolic murmur at the left lower sternal border. The chest was clear, and the rest of the systemic examination was within normal limits. Laboratory findings are summarized in .

An urgent transthoracic echocardiogram revealed a thickened tricuspid aortic valve with moderately restricted mobility and multiple large echogenic/mobile masses suggestive of vegetations (Video 3). A dilated aortic root and an aortic dissection were also noted (, ) and (Video 1). Additionally, there was moderate aortic stenosis and severe aortic regurgitation (Video 2), along with moderate tricuspid regurgitation and severe pulmonary hypertension. A TEE was not performed as the patient was transferred immediately for surgery.

Two sets of blood cultures were drawn, and both grew Streptococcus viridans. A diagnosis of infective endocarditis of the tricuspid aortic valve complicated by aortic dissection was made. The patient received intravenous Penicillin G (18 million units/day) and Gentamicin (3 mg/kg/day) for a total of 2 weeks. Repeat blood cultures were negative. The patient was stabilized and transferred emergently to a tertiary cardiac surgery unit, where he underwent successful surgical repair for the rupture.

Infective endocarditis (IE) is a serious medical condition with high morbidity and mortality, particularly when complicated by heart failure, systemic embolization, or peri-annular abscess formation. Aortic dissection (AD) is an exceptionally rare but life-threatening sequela of IE [⁵].

Although a bicuspid aortic valve (BAV) is a well-recognized substrate for both IE and aortopathy/dissection, our patient had a tricuspid valve, eliminating this common risk factor. Proposed mechanisms for IE-associated AD include direct microbial invasion of the aortic wall, activation of inflammatory cytokines, proteolytic tissue destruction, and hemodynamic stress from severe aortic regurgitation, which increases wall shear and predisposes to intimal tearing. When infection extends toward the aortic root, the combination of tissue destruction and pressure load may precipitate dissection [⁶,²].

The coexistence of acute AD and IE is exceedingly rare, with only a limited number of cases documented in the literature [⁷,⁸,⁹,⁶]. Published reports remain sparse and heterogeneous. For example, a recent case described simultaneous acute Type A AD and undiagnosed IE in a young adult with chronic kidney disease (CKD), presenting with chest and back pain and managed with aortic root replacement and six weeks of intravenous antibiotics [¹]. Our case differs by featuring no chest pain, a tricuspid valve, and no significant comorbidities, reinforcing that IE-associated AD can occur outside classic risk contexts and may lack typical pain syndromes.

Unlike the classical tearing chest pain seen in most cases of AD, our patient presented only with fever and progressive dyspnea. This highlights the need for a high index of suspicion, especially when cardiovascular findings such as diastolic murmurs, pulse deficits, and blood pressure discrepancies are present.

Initial evaluation for IE with transthoracic echocardiography (TTE) is common [¹⁰]. In our case, the definitive diagnosis of AD was confirmed by echocardiography, which demonstrated an intimal flap and aortic root dilation (, ) and (Video 1). The TEE was deferred as the TTE provided sufficient information. Early surgical intervention is crucial in the management of AD; without intervention, mortality increases by 1–2% per hour within the first 24–48 hours, reaching nearly 50% by the end of the first week [⁴]. Guidelines from ACC/AHA [¹¹], AATS [¹²], and EACTS/STS [¹³] support early surgery, individualized root and arch management, and emphasize valve replacement over repair in the presence of infection. Fortunately, our patient underwent timely surgical repair with aortic valve replacement, which was lifesaving.

Our case highlights a rare but serious complication of infective endocarditis—aortic dissection—presenting with atypical symptoms. In patients with suspected or confirmed IE, the absence of classic chest pain should not lower suspicion for AD when clinical findings suggest aortic regurgitation or perfusion disparity. Early use of TTE/TEE, rapid surgical engagement, and timely initiation of culture-directed antibiotics are critical steps that can be lifesaving in such scenarios.