Giant-Cell Aortitis-Induced Acute Aortic Insufficiency: An Underestimated Etiology.

BACKGROUND Acute aortic insufficiency can be secondary to multiple conditions, including infective endocarditis, aortic root pathologies (eg, dissection, aortitis), or traumatic injury. Aortitis involves a broad spectrum of disorders characterized by inflammatory changes in the aortic wall. This pathology can be subsequently classified depending on its etiology into inflammatory and infectious causes. Large-vessel vasculitis (giant-cell arteritis, Takayasu arteritis, and IgG4-related vasculitis) is the most common non-infectious causes of aortitis. Giant-cell aortitis usually lacks the classic clinical findings of giant-cell arteritis such as headache, visual symptoms, or jaw claudication, which can be a diagnostic challenge. However, clinicians should have a high index of suspicion, since this pathology can evolve into potentially life-threatening conditions, including aortic aneurysm, aortic wall rupture, and aortic acute dissection. CASE REPORT We present a case of a 76-year-old woman who presented to the Emergency Department (ED) with shortness of breath associated with orthopnea, paroxysmal nocturnal dyspnea, and mild productive cough with white sputum. A transthoracic echocardiogram demonstrated reduced left ventricular ejection fraction, dilated left ventricle, and severe aortic insufficiency. Cardiac catheterization revealed mild non-obstructive coronary arteries and severe aortic regurgitation. The surgical pathology report of the portion of the aorta was consistent with giant-cell aortitis. CONCLUSIONS In this article, we present a case of giant-cell aortitis as an unusual etiology of acute aortic insufficiency, which is most probably under-detected in clinical practice. In addition to describing the case, we aim to highlight the importance of proper ascending aorta evaluation in patients presenting with new-onset aortic regurgitation and heart failure to prevent associated morbidity and mortality.

A Rare Case of Eustachian Valve Endocarditis in a Young Male With Poorly Controlled Type 1 Diabetes Mellitus.

The eustachian valve (EV) is a vestigial structure found at the junction of the inferior vena cava and the right atrium, a remnant of the embryological sinus venosus that may persist throughout life. Right-sided infective endocarditis of the eustachian valve remains a distinctly rare and under-diagnosed entity. Commonly known risk factors of eustachian valve endocarditis (EVE) are intravenous drug use, in-dwelling intracardiac devices, and central lines, although more recently immunocompromised states, e.g. uncontrolled diabetes mellitus and old age, have been recognized as risk factors for the disease. Although Staphylococcus aureus has been the most commonly implicated organism, cases of infections with gram-negative organisms are emerging. We present a 47-year-old male with uncontrolled type 1 DM who initially presented to the ED with complaints of low back pain and dysuria and was later found to have eustachian valve endocarditis ultimately treated with intravenous antibiotics.

Acute-Hypoxemia-Induced Right-To-Left Shunting in the Presence of Patent Foramen Ovale.

Patent foramen ovale (PFO) is a common congenital abnormality of the heart. It results from incomplete closure of foramen ovale that persists in adulthood. Most individuals with PFO are asymptomatic and are discovered incidentally. The left atrial pressure is generally higher than the right atrial pressure, which prevents blood flow against the gradient; however, any medical condition that increases the pulmonary artery pressure can lead to reversal of blood flow from right to left by elevating right atrial pressure. We present a case of a 59-year-old female who presented with complaints of shortness of breath associated with bilateral lower-extremity edema and was found to have acute decompensated heart failure and atrial fibrillation. Transesophageal echocardiogram (TEE) with cardioversion was performed. Propofol was given for conscious sedation; however, the procedure was terminated as patient became hypoxemic and was noted to have moderately dilated right ventricle (RV) with hypokinesia and PFO with right-to-left shunting. It also demonstrated mild mitral regurgitation, mild left ventricular hypertrophy, and a left ventricular ejection fraction of 55-60%. In contrast to TEE findings, while the patient was having normal oxygen saturation, transthoracic echocardiogram showed left-to-right shunting instead of right-to-left and no RV hypokinesia was noted. In conclusion, this case draws attention to the relationship between acute hypoxemia and right-to-left shunting in a patient with PFO. This case illustrates and highlights the need for more prospective studies to establish a relationship between acute hypoxemia and right-to-left shunting in the presence of PFO.

Identification, characterization, and expression of sarcomeric tropomyosin isoforms in zebrafish.

Tropomyosin is a component of thin filaments that constitute myofibrils, the contractile apparatus of striated muscles. In vertebrates, except for fish, four TPM genes TPM1, TPM2, TPM3, and TPM4 are known. In zebrafish, there are six TPM genes that include the paralogs of the TPM1 (TPM1-1 and TPM1-2), the paralogs of the TPM4 gene (TPM4-1 and TPM4-2), and the two single copy genes TPM2 and TPM3. In this study, we have identified, cloned, and sequenced the TPM1-1κ isoform of the TPM1-1 gene and also discovered a new isoform TPM1-2ν of the TPM1-2. Further, we have cloned and sequenced the sarcomeric isoform of the TPM4-2 gene designated as TPM4-2α. Using conventional RT-PCR, we have shown the expression of the sarcomeric isoforms of TPM1-1, TPM1-2, TPM2, TPM3, TPM4-1, and TPM4-2 in heart and skeletal muscles. By qRT-PCR using both relative expression as well as the absolute copy number, we have shown that TPM1-1α, TPM1-2α, and TPM1-2ν are expressed mostly in skeletal muscle; the level of expression of TPM1-1κ is significantly lower compared to TPM1-1α in skeletal muscle. In addition, both TPM4-1α and TPM4-2α are predominantly expressed in heart. 2D Western blot analyses using anti-TPM antibody followed by Mass Spectrometry of the proteins from the antibody-stained spots show that TPM1-1α and TPM3α are expressed in skeletal muscle whereas TPM4-1α and TPM3α are expressed in zebrafish heart. To the best of our knowledge, this is by far the most comprehensive analysis of tropomyosin expression in zebrafish, one of the most popular animal models for gene expression study.