Abdominal Pain Reveals Hidden Heart Failure and Blood Clot in Young Man

A 38-year-old man walked into a hospital in Saudi Arabia complaining of two days of gnawing, colicky pain in his upper abdomen. He had no chest pain, no shortness of breath, no palpitations, and no exercise intolerance. He trained at the gym several times a week and considered himself entirely healthy, apart from a recent diagnosis of high blood pressure that he had not yet started treating. What clinicians found beneath this unremarkable surface was startling: his heart’s main pumping chamber was functioning at roughly a fifth of its normal capacity, and a blood clot was lodged at the apex of the left ventricle. The abdominal complaint that brought him to medical attention was, in effect, the only door through which a life-threatening cardiac condition could be reached.

The case, published in Clinical Case Reports, describes what the authors call a diagnostic interception. The man’s epigastric pain, which worsened after fatty meals and came with nausea, initially pointed toward acute cholecystitis, the inflammation of the gallbladder that is a common cause of upper abdominal discomfort. Yet abdominal ultrasonography told a more ambiguous story. It showed a gallbladder with a thickened, edematous wall measuring between 0.67 and 0.77 centimeters and mild free fluid around the liver, but no gallstones and no sludge. Critically, the same study picked up an incidental right-sided pleural effusion, an accumulation of fluid in the chest lining that had nothing obvious to do with the biliary system.

That single incidental finding set off a diagnostic chain reaction. A chest radiograph followed, revealing cardiomegaly with a globular cardiac silhouette consistent with a dilated left ventricle. Blood tests added another clue: the patient’s B-type natriuretic peptide, or BNP, a hormone released when the heart is under strain, was moderately elevated at 443.5 picograms per milliliter, far above the reference value of less than 28.9. Isolated biliary pathology does not typically raise BNP. Meanwhile, his liver enzymes told a story of congestion rather than infection: alkaline phosphatase was markedly elevated at 382 units per liter and total bilirubin at 21.3 micromoles per liter, but inflammatory markers were only mildly raised, C-reactive protein at 12.8 milligrams per liter, and serial troponin measurements, the proteins released when heart muscle dies, remained within normal limits throughout.

Electrocardiography was the next step, and it showed new ST-segment and T-wave abnormalities in the lateral leads when compared with a prior baseline recording that had been entirely normal. This combination of findings, elevated BNP, an enlarged heart on imaging, pleural fluid, and fresh electrical changes, in a patient with no fever and no signs of infection, redirected the diagnostic pathway away from the gallbladder and toward the heart. Urgent echocardiography delivered the answer: severely reduced left ventricular systolic function with an ejection fraction of approximately 20 percent, severe global hypokinesia, Grade I diastolic dysfunction, mild right ventricular impairment, elevated filling pressures, a small pericardial effusion without tamponade, and a dilated inferior vena cava measuring 3 centimeters. The diagnosis was newly discovered heart failure with reduced ejection fraction, or HFrEF.

The mechanism behind the abdominal symptoms is well described in the cardiohepatic literature. When the failing heart cannot pump efficiently, pressure backs up through the right side of the circulation into the hepatic and portal venous systems. This elevated central venous pressure produces congestive hepatopathy, gallbladder wall edema, pericholecystic fluid, and a cholestatic pattern of liver enzyme abnormalities that can closely mimic acute cholecystitis both clinically and radiologically. Autonomic connections between the cardiac and biliary systems also exist, with vagally mediated reflexes capable of producing cardiac manifestations from biliary stimulation, but in heart failure presenting through the abdomen, the dominant and best-supported mechanism is hemodynamic. In this patient, the absence of gallstones, a negative Murphy’s sign, an afebrile state, and only mildly elevated inflammatory markers made infective cholecystitis unlikely, and surgical intervention was deferred.

Review of the patient’s prior records revealed blood pressure readings as high as 188 over 130 millimeters of mercury. In the absence of another identified cause at that stage, markedly uncontrolled hypertension was considered the most likely contributor to the cardiomyopathy. He was started on guideline-directed medical therapy, including bisoprolol, candesartan, spironolactone, and dapagliflozin, and transferred to a tertiary cardiac center for advanced evaluation. There, cardiac magnetic resonance imaging confirmed the severe systolic dysfunction and made a discovery that changed management: a left ventricular apical thrombus measuring 1.5 by 0.7 centimeters. Left ventricular thrombus is a recognized complication of HFrEF, occurring with higher frequency in patients whose ejection fractions fall below 25 percent and who have apical wall motion abnormalities, precisely the profile this patient presented.

The cardiac MRI also added etiologic nuance that echocardiography alone could not provide. Late gadolinium enhancement, a technique that highlights areas of scarred or fibrotic myocardium, showed a focus in the basal inferior wall with a pattern considered consistent with a possible embolic ischemic substrate rather than the diffuse nonischemic fibrosis typically associated with hypertensive or idiopathic dilated cardiomyopathy. Global myocardial native T1 time and extracellular volume fraction were normal, excluding significant diffuse fibrosis, and there was no evidence of myocardial edema or iron overload, with a T2 star value of 33 milliseconds. The treating team considered the cardiomyopathy predominantly nonischemic, attributing the basal inferior enhancement to a possible embolic event in the context of the known apical thrombus. However, formal coronary angiography was not performed, so the etiology remains presumptive. Anticoagulation was initiated with heparin and transitioned to apixaban at 5 milligrams twice daily, a decision that would not have been made had the presentation been managed as biliary disease alone.

The recovery trajectory was striking. At approximately two weeks, echocardiography showed the ejection fraction had improved to between 25 and 30 percent, and the abdominal symptoms had resolved completely without any biliary intervention. At around ten weeks, the ejection fraction had climbed further to 38 percent on three-dimensional echocardiography, BNP had normalized to 32.3 picograms per milliliter, and the apical thrombus had completely resolved on repeat imaging, allowing anticoagulation to be discontinued. At six-month outpatient review, echocardiography demonstrated a mildly dilated left ventricle with moderate global hypokinesia, preserved diastolic filling pressures, and no pericardial effusion. The patient was clinically compensated on a regimen that included sacubitril/valsartan, bisoprolol, spironolactone, dapagliflozin, nifedipine extended-release, atorvastatin, and apixaban, with follow-up planned in a further five months.

What makes this case clinically significant is not the cardiohepatic mimic itself, which is already documented in the literature, including in young patients, but the specific combination it represents: clinically silent severe HFrEF, a left ventricular apical thrombus, an abdominal presentation in a young asymptomatic patient, and subsequent complete thrombus resolution with sustained ventricular recovery, all documented with cardiac MRI tissue characterization. The authors note that no report they identified described this exact combination. The patient’s functional compensation in the setting of such severe ventricular dysfunction reflects the capacity of young patients to upregulate compensatory mechanisms, including sympathetic activation, peripheral vascular adaptation, and skeletal muscle efficiency, to a degree that masks even profoundly impaired cardiac function. That same resilience is what allows severe disease to accumulate undetected, because the absence of typical symptoms never prompts a cardiac evaluation.

The diagnostic lesson is straightforward and potentially lifesaving. In any patient presenting with abdominal pain and hepatobiliary findings, a moderately elevated BNP, unexplained cardiomegaly, or pleural effusion should prompt urgent echocardiography before surgical referral, regardless of the patient’s age or apparent fitness. When severe left ventricular dysfunction is identified, cardiac MRI adds diagnostic value beyond thrombus detection: tissue characterization through late gadolinium enhancement, T1 mapping, and T2 star imaging can help differentiate ischemic from nonischemic substrate, identify inflammatory or infiltrative disease, and assess the extent of fibrosis, all of which bear on prognosis, likelihood of recovery, and management decisions. The favorable outcome here, with the ejection fraction rising from 20 to 38 percent and BNP falling from 443.5 to 32.3, is consistent with the responsiveness of nonischemic or hypertensive cardiomyopathy to guideline-directed medical therapy when initiated before irreversible fibrosis takes hold. Whether that recovery reflects the underlying reversibility of the condition, the treatment effect, or both cannot be determined from a single case, but the temporal association with therapy is clear. For young, physically active patients who seem the least likely candidates for heart failure, an abdominal complaint may be the first and only opportunity for diagnosis, and each incidental finding along the way deserves to be read as part of a pattern rather than dismissed in isolation.

Subject of Research: A case report of clinically silent severe heart failure with reduced ejection fraction and left ventricular thrombus presenting as abdominal pain in a young asymptomatic patient

Article Title: Abdominal Pain as the First Presentation of Severe Heart Failure With Reduced Ejection Fraction and Left Ventricular Thrombus in a Young Asymptomatic Patient: A Diagnostic Interception

Article References: Alarfaj, M. O., Alsuwailem, B. S., Aljeezan, M. K., Alhlibi, B. S., Haya, M. M. B., Alnaaim, A. A., & AlTaweel, M. O. (2026). Abdominal Pain as the First Presentation of Severe Heart Failure With Reduced Ejection Fraction and Left Ventricular Thrombus in a Young Asymptomatic Patient: A Diagnostic Interception. Clinical Case Reports, 14(10), Article e73699. https://doi.org/10.1002/ccr3.73699

Image Credits: AI Generated

DOI: 10.1002/ccr3.73699

Keywords: heart failure, reduced ejection fraction, left ventricular thrombus, congestive hepatopathy, cardiac MRI, diagnostic interception, hypertension, echocardiography, BNP, gallbladder mimic, cardiomyopathy, anticoagulation