A systolic murmur best heard at the aortic area with radiation to the neck is considered a hallmark of aortic stenosis. We report a patient with this auscultatory pattern in whom investigation revealed an unexpected diagnosis. Accompanying symptoms reinforced the initial suspicion, adding another layer of complexity to the diagnostic process. This case highlights the limitations of relying solely on symptom profile and murmur topography, and underscores the importance of comprehensive physical examination and diagnostic imaging in evaluating valvular heart disease.

Acquired cardiovascular diseases are recognized as a major age-related cause of morbidity and mortality in captive squirrel monkeys (Saimiri spp.). An 11-year-old intact male black-capped squirrel monkey (Saimiri boliviensis boliviensis) was presented following a syncopal episode associated with respiratory distress, abdominal distension, and peripheral edema. Upon presentation, the animal appeared thin and debilitated. Physical examination revealed respiratory distress with paradoxical breathing, abdominal distension, peripheral edema of the hind limbs, and hypothermia. Thoracic auscultation identified a loud systolic murmur over the left hemithorax and diffuse pulmonary crackles. Thoracic radiographs demonstrated severe cardiomegaly and perihilar pulmonary interstitial pattern consistent with cardiogenic pulmonary edema. Two-dimensional echocardiography revealed hyperechoic papillary muscles, thickened and restricted mitral valve leaflets, and shortened chordae tendineae with secondary severe left atrial and ventricular dilation. Doppler echocardiography demonstrated severe mitral regurgitation. Congestive heart failure secondary to mitral valve dysplasia was diagnosed. Treatment with diuretics and vasodilators resulted in transient clinical improvement followed by rapid deterioration of the patient's condition; therefore, euthanasia was elected. Gross pathological and histopathological examinations revealed thickened and irregular mitral valve leaflets with hypoplastic chordae tendineae associated with severe left-sided cardiac enlargement. To the authors' knowledge, this is the first report describing mitral valve dysplasia in an adult squirrel monkey. This report expands the spectrum of cardiovascular diseases described in squirrel monkeys and highlights the importance of advanced cardiac imaging in the diagnosis of rare congenital cardiac defects in non-human primates.

Williams syndrome (WS) is a rare microdeletion disorder affecting chromosome 7q11.23, including the ELN gene, which encodes elastin. Haploinsufficiency of ELN leads to vascular abnormalities, such as supravalvular aortic stenosis (SVAS), pulmonary stenosis, and coronary artery disease. SVAS can also occur in isolation due to heterozygous loss-of-function variants in ELN, independent of the broader WS deletion. We present a case of a term neonate with a Grade 4/6 systolic ejection murmur who underwent echocardiography, revealing severe supravalvular pulmonary stenosis, branch pulmonary artery stenosis, and mild SVAS. Due to these WS-like features, a chromosomal microarray was performed, which ruled out WS. Cardiac catheterization for pulmonary artery balloon angioplasty was complicated by ventricular fibrillation, requiring resuscitation. Angiography identified coronary artery stenosis. Intraoperative cardiac instability raised concerns for an ELN-related vasculopathy. Whole-exome sequencing (WES) revealed an ELN frameshift mutation in exon 6. This case describes a neonate with a WS-like cardiovascular phenotype but no WS-associated deletion, instead harboring a heterozygous pathogenic ELN loss-of-function variant consistent with isolated SVAS, thereby challenging genotype-phenotype correlations.

The conventional view holds that left ventricular (LV) apical ballooning in stress cardiomyopathy is caused by a hyperadrenergic state related to emotional or physical stress. However, some suggest ballooning also occurs in obstructive hypertrophic cardiomyopathy (HCM) when obstruction becomes severe. Nearly all cases of apical ballooning in HCM were reported in patients with LV outflow tract obstruction. Herein, we present a case due to mid-ventricular obstruction.

Tricuspid regurgitation (TR) is increasingly recognized as an important cause of right-sided heart failure and adverse clinical outcomes. Although severe TR typically presents with a holosystolic murmur, advanced disease may produce atypical findings that obscure the diagnosis. Lancisi's sign, characterized by prominent systolic jugular venous pulsations, remains an important but underrecognized bedside clue to severe TR. We present the case of a 60-year-old man with a remote history of presumed infective endocarditis who presented with progressive dyspnea, anasarca, and peripheral edema. Physical examination revealed marked systolic jugular venous pulsations consistent with Lancisi's sign but no audible cardiac murmur. Transthoracic echocardiography demonstrated complete degeneration of the tricuspid valve leaflets, torrential TR, massive right-sided chamber dilation, and right atrial ventricularization. Doppler interrogation confirmed rapid pressure equalization between the right atrium and right ventricle. Given the advanced right-sided remodeling and evidence of end-organ involvement, the patient was deemed unsuitable for surgical or transcatheter intervention and was managed medically. This case highlights the diagnostic value of careful physical examination and illustrates how severe TR may present without its classic auscultatory findings. Early recognition of bedside signs such as Lancisi's sign may facilitate timely diagnosis before progression to irreversible right-sided heart failure.

A 14-year-old neutered male Toy Poodle was presented for elective bilateral phacoemulsification surgery. After initial physical examination at the hospital, oral trazodone (5 mg kg[-1]) was given approximately 2 hours before anaesthesia to facilitate preoperative handling. Approximately 1 hour after trazodone and before anaesthetic premedication, a previously undocumented grade 3/6 left apical systolic heart murmur was auscultated during repeat physical examination. Focused echocardiographic assessment revealed subjectively reduced left ventricular internal dimensions with an appearance suggestive of concentric hypertrophy. No overt clinical evidence of dehydration was identified, although serum biochemistry revealed a mild increase in symmetric dimethylarginine concentration (16 μg dL[-1]; reference interval 0-14 μg dL[-1]). Elective anaesthesia and surgery were postponed, and the dog was hospitalised overnight for intravenous fluid therapy. Repeat cardiovascular assessment approximately 22 hours after the initial trazodone dose revealed resolution of the heart murmur and normal left ventricular internal dimensions on echocardiography. Similar cardiovascular findings did not recur after subsequent trazodone dosing under conditions of improved intravascular volume. This case describes transient cardiovascular changes temporally associated with trazodone use in a geriatric dog undergoing preanaesthetic assessment and highlights the potential influence of intravascular volume status on interpretation of cardiovascular findings.

Pediatric heart murmurs are common findings during physical examination, but only a small number of cases require intervention. This case report highlights a routine physical examination for a 10-year-old male patient that revealed a grade III/VI harsh systolic murmur heard in all areas of auscultation and a fixed split S2. A subsequent transthoracic echocardiogram showed an atrial septal defect that required catheter-based closure. This case proved to be one of the few cases in which urgent treatment of the heart murmur is required, and it helps highlight the features of pathologic murmurs that should prompt further evaluation.

Iatrogenic arteriovenous (AV) fistula is a rare but treatable cause of high-output heart failure that can mimic restrictive cardiomyopathy and may lead to inappropriate listing for heart transplantation.

Severe mitral stenosis is a valvular heart disease that obstructs blood flow from the left atrium to the left ventricle, leading to impaired ventricular filling, left atrial dilatation, atrial fibrillation, and thromboembolic events. We report the case of a female patient who presented with shortness of breath (NYHA Class-II) for six months. On examination, a low-pitched murmur was heard at the apex; other systemic examination findings were unremarkable. TTE/TEE revealed left atrial dilatation with LAVI of 120 ml/m2, a large left atrial thrombus, severe rheumatic mitral stenosis, and moderate mitral regurgitation with preserved systolic function, leading to MVR. The thrombus was firmly adherent; after failed attempts to create a plane, it was successfully removed using a polypropylene needle. The unusually small mitral annulus was managed by creating fenestrations. This case highlights the importance of preoperative evaluation and individualized surgical approaches for improved outcomes.

BACKGROUND Heyde syndrome is an uncommon clinical entity characterized by severe aortic stenosis (AS) and acquired von Willebrand syndrome, typically presenting with recurrent gastrointestinal bleeding secondary to angiodysplasia. Although most reported cases involve isolated gastrointestinal bleeding, the coexistence of thromboembolic events is exceedingly rare and poses a significant therapeutic challenge in balancing hemostatic and anticoagulant strategies. CASE REPORT We report a 70-year-old woman who initially presented with massive hematochezia and subsequently developed dyspnea, requiring hospitalization. Physical examination revealed a prominent systolic murmur over the aortic area. Transthoracic echocardiography confirmed severe AS, with an aortic valve area of 0.8 cm[2] and a mean transvalvular pressure gradient of 71 mm Hg. Together with profound anemia (hemoglobin 44 g/L) and markedly reduced von Willebrand factor ristocetin cofactor activity (vWF: RCo, 25.3%), these findings supported the diagnosis of Heyde syndrome. During the preprocedural evaluation for transcatheter aortic valve replacement (TAVR), acute pulmonary embolism was incidentally identified on computed tomography pulmonary angiography. After hemostatic stabilization, anticoagulant therapy was cautiously initiated, resulting in complete resolution of the pulmonary embolism after 1 month. Given the elevated surgical risk (EuroSCORE II, 8.05%), the patient underwent successful TAVR. Following the procedure, the transvalvular pressure gradient normalized (mean, 13.8 mm Hg), with restoration of normal vWF activity. CONCLUSIONS This case underscores the therapeutic complexity of simultaneously managing hemorrhagic and thrombotic risks in Heyde syndrome. TAVR remains the definitive treatment for acquired von Willebrand syndrome, while a staged, individualized anticoagulation approach is crucial in patients with concomitant thromboembolic complications. Correcting the underlying AS remains the cornerstone of management.

Ventricular septal defect (VSD) is a rare and sparsely reported congenital heart disease in guinea pigs that arises from embryonic maldevelopment or misalignment of the interventricular septum, leading to an interventricular communication. A 2.5-year-old intact male guinea pig (Cavia porcellus) that weighed 0.713 kg was presented for a fractured right mandibular incisor, and an incidental grade V/VI right parasternal systolic murmur was detected in the absence of clinical signs of cardiac disease. Radiographic imaging revealed an enlarged cardiac silhouette in the ventrodorsal thoracic radiograph (10.0) with a normal lateral vertebral heart scale of 7.2. Echocardiography identified a small restrictive perimembranous VSD with left-to-right shunting and a peak ventricular pressure gradient of 80 mmHg, without additional morphologic or functional cardiac abnormalities. At the time of publication, this animal had remained stable without medical or surgical intervention and had undergone 12 anesthetic events for occlusal adjustments related to a variety of dental abnormalities resulting in malocclusion without significant complications. Similar to domestic small animal species with restrictive VSDs, guinea pigs can remain subclinical and stable under repeated anesthetic events.