Coronary subclavian steal syndrome causing myocardial Infarction.

Coronary subclavian steal syndrome (CSSS) is a rare complication of the internal mammary artery (IMA) grafting in coronary artery bypass surgery. The technical definition is myocardial ischemia due to the reduced flow of blood, or flow reversal in the IMA graft. This in most cases results from hemodynamically significant proximal subclavian artery stenosis. The clinical presentation is variable and ranges from unstable angina to myocardial infarction, and in some cases, sudden cardiac arrest. CSSS is an entity that is hard to diagnose if one is not actively looking for it. The clinical diagnosis is often complicated, and the prevalence of the disorder is frequently underestimated. In this case presentation, we report a case of myocardial infarction that resulted from significant proximal subclavian artery stenosis.

Hemopericardium in a Sirolimus-Treated Renal Transplant Patient.

Sirolimus is an immunosuppressant frequently prescribed to prevent graft-vs-host disease in renal transplant patients. Pericardial effusion is recognized as a rare and potentially lethal side effect of this medication. Hemopericardium, specifically, is an even rarer complication that has yet to be reported in the literature. We report the first case of sirolimus-induced hemopericardium in a renal transplant patient.

Gerbode defect formation two decades after tetrology of fallot repair.

Although most intracardiac defects are congenital, a small fraction may be acquired during life. The Gerbode defect is an abnormal anatomical connection between the left ventricle and the right atrium. We describe herein a patient who initially underwent repair of tetralogy of Fallot (TOF). Years after TOF repair, he developed severe dyspnea. Extensive evaluation revealed that he had developed a Gerbode defect. Very few cases of acquired Gerbode defect have been previously reported. Management options are predominantly surgical interventions.

Sternal osteomyelitis by Gordonia Bronchialis in an immunocompetent patient after open heart surgery.

Gordonia is a catalase-positive, aerobic, nocardioform, Gram-positive staining actinomycete that also shows weak acid-fast staining. Several Gordonia species are commonly found in the soil. The bacterium has been isolated from the saliva of domesticated/wild dogs as well. In hospitalized patients, most commonly it is found in the setting of intravascular catheter-related infections. However, recent reports show that it is being increasingly isolated from sternal wounds, skin/neoplastic specimens and from pleural effusions. Gordonia shares many common characteristics with Rhodococcus and Nocardia. Ergo, it is commonly misrecognized as Nocardia or Rhodococcus. Since this pathogen requires comprehensive morphological and biochemical testing, it is often difficult and cumbersome to isolate the species. Broad-range Polymerase Chain Reaction (PCR) and sequencing with genes like 16S rRNA or hsp65 are used to correctly identify the species. Identification is essential for choosing and narrowing the right antimicrobial agent. Herein, we report our experience with a patient who presented with sternal osteomyelitis after infection with this elusive bug.

The dilemma of the "ischemic-looking" electrocardiogram: Pulmonary embolism or acute coronary syndrome?

Pulmonary embolism (PE) may be potentially fatal if not diagnosed and treated in time. Although specific electrocardiogram (ECG) findings often suggest the diagnosis of PE, occasionally, the ECG may mimic that of an acute coronary syndrome (ACS). We report an interesting case of a 45-year-old female presenting with sudden onset chest pain and shortness of breath with widespread ST depression in anterior precordial leads. Although initially treated and referred as a case of ACS, careful analysis of the ECG and subsequent echocardiography and computed tomography imaging confirmed the diagnosis of PE. Intensivists and cardiologists need to be aware that diagnostic dilemma between PE and ACS is not uncommon due to such "ischemic-looking" ECG as well as elevated troponin levels in both conditions. The use of multimodality imaging techniques is helpful in arriving at the correct diagnosis.

Venous Thromboembolism and Cancer.

PURPOSE OF REVIEW: This review aims to summarize the epidemiology, current pathophysiologic understanding, and state-of-the-art treatment of venous thromboembolism (VTE) in cancer patients. RECENT FINDINGS: The risk of VTE varies among cancer patients. Recently introduced prediction models better identify those at high risk of VTE. New mechanisms underlying hypercoagulability in cancer have been uncovered. Initial data on the efficacy of direct oral anticoagulants (DOACs) compared with low-molecular weight heparin to treat VTE in patients with cancer are promising. However, they may be associated with higher risk of gastrointestinal bleeding. VTE causes significant morbidity and mortality in cancer patients. Our understanding of the mechanisms of VTE, including those associated with cancer treatments, has significantly grown. The assessment of the benefit/risk balance of VTE treatment remains challenging in many patients with cancer. The introduction of DOACs has expanded treatment options, but knowledge on their efficacy and safety is incomplete.

Jet lag: Heuristics and therapeutics.

Jet lag is one of those common medical problems, to which most people don't give a serious thought. However, it is intricately intertwined with our normal circadian rhythm. It is classified as a sleep disorder. There is also a dearth of good scientific literature, not to mention clinical trials on the subject. Slowly but steadily, the scientific community is realizing the various deleterious health effects of jet lag and is devising innovative methods to counter them. This narrative review touches upon the etiopathogenesis, clinical manifestations and therapeutic strategies effective against the nagging problem of jet lag.

Unusual Sign from an Unusual Cause: Wellens' Syndrome due to Myocardial Bridging.

It is vital to recognize correctly, chest pain of cardiac etiology. Most commonly, it is because of blood supply-demand inequity in the myocardium. However, the phenomenon of myocardial bridging as a cause of cardiac chest pain has come to attention reasonably recently. Herein, a coronary artery with a normal epicardial orientation develops a transient myocardial course. If the cardiac muscle burden is substantial, the respective artery gets compressed during each cycle of systole, thereby impeding blood flow in the artery. Hence, myocardial bridging has been attributed to as a rare cause of angina. In this case report, the authors discuss a patient in whom myocardial bridging turned out to be an elusive cause of angina. We wish to underscore the importance of being clinically mindful of myocardial bridging when assessing a patient with angina.

Cardiogenic Shock: A Rare Complication of Influenza.

We have presented a case of 41-year-old male who presented to the hospital with worsening shortness of breath, fatigue and flu-like symptoms. On admission to hospital, the patient was in severe cardiogenic shock secondary to acute perimyocarditis. He was admitted to the cardiac intensive care unit for close monitoring and aggressive hemodynamic support. Influenza B antigen was detected in nasopharyngeal aspirate and the patient was started on oseltamivir. The patient's cardiac function improved significantly in few days and he was discharged home in stable condition with normal ejection fraction.

New daily persistent headache: An evolving entity.

New daily persistent headache (NDPH) is characterized by an abrupt onset of headache that becomes a daily entity, is unremitting and continuous from the onset, and lasts for more than 3 months. Dr Walter Vanast first described NDPH in the year 1986. Originally, it was proposed as a chronic daily headache but it was placed under "other primary headaches" in the International Classification of Headache Disorder Second Edition (ICHD 2nd edition). However, with evolving literature and better understanding of its clinical characteristics, it was classified as a "chronic daily headache" in the ICHD 3rd edition beta. There are still many knowledge-gaps regarding the underlying cause, pathophysiology, natural history and treatment of NDPH. This review tries to revisit the entity and discusses the current status of understanding regarding NDPH.

Strongyloides Hyperinfection and Miliary Tuberculosis Presenting with Syndrome of Inappropriate Antidiuretic Hormone Secretion in a Malnourished Patient.

Strongyloides stercoralis (S. stercoralis) is an intestinal nematode endemic to tropical regions. An accelerated infection, known as a hyperinfection, occurs in immunocompromised patients, most commonly those treated chronically with glucocorticoids or those who have human T cell leukemia virus-1 (HTLV-1) infection. We describe a 67-year-old Hispanic female who presented with complaints of decreased oral intake and fatigue since three months. Hyponatremia on initial presentation was attributed to syndrome of inappropriate antidiuretic hormone (SIADH) secretion and managed with fluid restriction. Computed tomography (CT) of the chest revealed multiple pulmonary nodules suggestive of miliary tuberculosis, however, sputum acid-fast bacilli (AFB) smears were negative. Fiberoptic bronchoscopy with bronchoalveolar lavage (BAL) was performed and specimens sent for AFB testing. A concurrent endoscopy with biopsy was done to evaluate dysphagia. Both respiratory and gastrointestinal (GI) specimens were positive for Strongyloides stercoralis. Treatment with ivermectin and prophylactic antibiotics was started. The patient developed septic shock and had multiple episodes of gastrointestinal bleeding. Despite aggressive management, she expired. Subsequently, cultures for Mycobacterium tuberculosis (MTB) were positive and the autopsy demonstrated evidence of MTB infection in the lungs, liver, and lymph nodes. This case illustrates the importance of considering co-infection with Strongyloides stercoralis in patients with MTB, both associated with depressed cellular immunity.

Severe Pulmonary Hypertension Due to Adult-Onset Still's Disease.

A 29-year-old female with adult-onset Still's disease (AOSD) presented with progressive shortness of breath both on rest and on exertion, increased abdominal girth, and swelling in both legs. She was on oral prednisone and was recently started on canakinumab (interleukin-1 antagonist) for joint pain and rash of AOSD. Echocardiogram showed severely dilated right ventricle, dilated pulmonary artery, moderately reduced right ventricular systolic function, but with normal left ventricular systolic function. Computed tomography with contrast ruled out pulmonary embolism. Blood tests ruled out other rheumatologic diseases. The patient was diagnosed with right-sided heart failure likely secondary to AOSD. Right heart catheterization was needed but could not be performed because of severely dilated pulmonary artery. The patient was transferred to a higher center for further management and possible cardiopulmonary transplant.