EUHM Report: What syndromes are associated with Pulse Temperature Disassociation?

The Bottom Line: The mechanisms for fever-induced bradycardia are not completely understood. It is well known that many infectious agents can cause acute myocarditis and induce cardiac conduction abnormalities. One study suggested that relative bradycardia due to a specific disease has no predictive value in making a diagnosis. However, another  suggests that relative bradycardia in a single patient can be helpful in arriving at a tentative diagnosis.

Mittal J, Estiverne C, Kothari N, Reddi A. Fever and Relative Bradycardia: A Case Presentation and Review of the Literature. Int J Case Rep Short Rev. 2015;1(1): 004-008.

In many noninfectious and infectious conditions, the heart rate does not increase with a rise in temperature. This phenomenon is called pulse-temperature deficit which many clinicians refer to as relative bradycardia. A caveat to this rule is that a patient must have a temperature of at least 102 F in order to better appreciate this pulse temperature relationship

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Dressler Conference: Review of polymyositis

The Bottom Line: Inflammatory idiopathic myopathies (IIM) are a group of rare autoimmune diseases characterized by proximal skeletal muscle weakness, raised muscle enzymes and extramuscular organ involvement, most frequently the lungs, resulting in interstitial lung disease (ILD). Numerous autoantibodies are associated with the disease, many linked to different clinical phenotypes.  Polymyositis predominantly presents with proximal symmetrical muscle weakness, while dermatomyositis is characterized by skin and muscle involvement; both are associated with extramuscular features.

Clark, K., & Isenberg, D. (n.d.). A review of inflammatory idiopathic myopathy focusing on polymyositis. European Journal of Neurology., 25(1), 13-23.

The main aims of treatment are to suppress inflammation, improve muscle power and prevent chronic damage to muscles and extramuscular organs. However, there is a lack of robust data to guide treatment.  Glucocorticoids remain the mainstay of treatment in IIM. Initial dosing is approximately 0.5 mg/kg of prednisolone, but the many side effects of steroids encourage a reducing regime over the first 2 months.  Methotrexate and azathioprine are often used as first line disease modifying anti-rheumatic drugs. A Cochrane review found insufficient evidence of improved efficacy using one DMARD (methotrexate, azathioprine or cyclosporine) in combination with corticosteroids in preference to another.

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VA Report: Dysphagia in the setting of myocardial infarction

Examples for extrinsic esophageal compression are found in inflammatory, postoperative and neoplastic mediastinal diseases, but also in substernal strumae, cervical spondylitis and vertebral osteophytes. Vascular esophageal compression syndromes are typically caused by an aberrant origin of the right subclavian artery far left in the aortic branch and course of this “A. lusoria” anterior or posterior of the esophagus. In addition, similar forms of esophageal compression can result from a congenital right-sided aorta, aortic aneurysms and conditions of left atrial enlargement.

Werner, C., Rbah, R., & Böhm, M. (n.d.). Cardiovascular dysphagia. Clinical Research in Cardiology : Official Journal of the German Cardiac Society., 95(1), 54-56.

Radiological imaging revealed an extrinsic esophageal compression as the cause of the patient’s complaints, for example, due to a mediastinal tumor. However, computed tomography of the chest showed a rare case of cardiovascular compression as the cause of dysphagia in this case. The patient turned down the option of endoscopic examination at the time.

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EUH Dressler Case Conference: Review of Myocardial Infarction and Myocardial Ischemia

The Bottom Line: Myocardial infarction (MI) is caused by prolonged myocardial ischemia, a condition where atherosclerotic plaques limit coronary flow reserve. About 25% of patients exhibiting symptoms of acute cardiac ischemia (ACI) will have a myocardial infarction.


Lanza GA, Crea F. Overview of Management of Myocardial Ischemia: a Mechanistic-Based Approach. Cardiovasc Drugs Ther. 2016 Aug;30(4):341-349.

Simel DL, Goodacre SW, Kristin L. “Myocardial Infarction”. The Rational Clinical Examination: Evidence-Based Clinical Diagnosis. Eds. David L. Simel & Drummond Rennie. New York, NY: McGraw-Hill.

Diagnosing a patient with MI should be based on whether the patient is exhibiting symptoms (i.e. chest pain, shortness of breath, cardiac arrest, abdominal pain) rather than whether the patient exhibits any risk factors for MI. The most beneficial methods to detect acute myocardial infarction are by observing changes in the Q waves or observing ST-segment elevation or depression on an ECG by the bedside; if ECG results are normal or non-diagnostic, measuring the patient’s symptoms using predictive models can be useful in diagnosing MI.


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VA Report: What is the etiology and treatment options for Rapidly progressive crescentic glomerulonephritis?

The Bottom Line:  Early treatment is of paramount importance for patients with crescentic GN. The current approach is based on a combination of corticosteroids and cytotoxic drugs with the aims of quenching the active inflammation and abating the cellular response and the antibody production

The etiology and the initial pathogenetic factors are different in the three types, but the final mechanisms leading to crescent formation and the renal symptoms and signs are similar.

Moroni, G., & Ponticelli, C. (n.d.). Rapidly progressive crescentic glomerulonephritis: Early treatment is a must. Autoimmunity Reviews, 13(7), 723-729.

The term crescentic glomerulonephritis (GN) refers to a pathologic condition characterized by extracapillary proliferation in > 50% of glomeruli. Clinically crescentic GN is characterized by a nephritic syndrome rapidly progressing to end stage renal disease (ESRD).

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EUH Morning Report: Review of microscopic colitis

Bottom Line: “Microscopic colitis is a common cause of chronic watery diarrhea, particularly in the elderly. The accompanying symptoms, which include abdominal pain and fatigue, can markedly impair patients’ quality of life. Diagnosis is based upon characteristic histologic findings of the colonic mucosa….Two recent randomized studies have confirmed the effectiveness of oral budesonide for both induction and maintenance treatment of microscopic colitis and is now endorsed by the American Gastroenterological Association as first-line treatment.”

Reference: Cotter TG, Pardi DS. Current approach to the evaluation and management of microscopic colitis. Curr Gastroenterol Rep. 2017 Feb;19(2):8.

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EUH Dressler Case Conference: What is the definition of heart failure with mid-range ejection fraction (HFmrEF), which is also called intermediate ejection fraction and borderline heart failure with preserved left ventricular (LV) ejection fraction (HFpEF)? Do patients benefit from typical HFrEF therapies?

Bottom Line: In a meta-analysis, Zheng, Chan, Nabeebaccus, et al. state, “The latest European Society of Cardiology guidelines introduced the term heart failure with mid-range ejection fraction (HFmrEF), categorising an intermediate group of patients with an LV ejection fraction of between 40% and 49%, with HFpEF defined as an LV ejection fraction ≥50% with the same echocardiographic criteria. The American College of Cardiology defines HFpEF as an LV ejection fraction >40%, with anything from 41% to 49% as borderline HFpEF.” Dressler reviewed the aforementioned article and states, “In 6 randomized trials (≈1300 patients), β-blockers, compared with placebo, significantly lowered early mortality (18% vs. 20%). In 15 randomized trials (>13,000 patients), HFpEF patients who received any drug class that improves [heart failure with reduced ejection fraction (HFrEF) outcomes were significantly less likely to be hospitalized (14% vs. 16% with placebo; number needed to treat, 64), but no individual medication class yielded significant improvements.” Drug classes that are typically used to treat HFrEf and were evaluated in the meta-analysis include β-blockers, angiotensin-converting–enzyme inhibitors, angiotensin-receptor blockers, and mineralocorticoid-receptor antagonists.
Zheng SL, Chan FT, Nabeebaccus AA, et al. Drug treatment effects on outcomes in heart failure with preserved ejection fraction: a systematic review and meta-analysis. Heart. 2017 Aug 5.
Dressler DD. Do any meds improve outcomes in heart failure with preserved ejection fraction. N Engl J Med J Watch. 2018 Jan 16.

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