In Morgan and Nadas’s seminal study they reported that sweating was greater at rest in HF patients compared with controls. Moreover, recent studies suggest that HF patients have similar sweating responses to controls when exposed to passive wholebody heating (Table 1).
Table 1. A Summary of Findings From Key Studies to Date Examining Thermoregulation in the Context of HF
Balmain, B., Sabapathy, S., Jay, O., Adsett, J., Stewart, G., Jayasinghe, R., & Morris, N. (n.d.). Heart Failure and Thermoregulatory Control: Can Patients With Heart Failure Handle the Heat? Journal of Cardiac Failure., 23(8), 621-627.
A common finding among studies examining thermoregulation in the context of HF to date is that HF patients appear to demonstrate impaired heat-induced increases in SkBF compared with controls. Although the mechanisms responsible for impaired SkBF in HF are not yet well understood, it may be argued that the compensatory activation of neurohumoral mechanisms that increase with severity of the condition at least partially contribute to the blunted heat-induced rise in SkBF in HF patients
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
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.
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.
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.
Bottom Line: In patients with pericardial effusion, the water bottle sign appears when the chest x-ray’s cardiac silhouette has a globular shape that looks like a water bottle as the result of slowly accumulating fluid. In the screenshot from YouTube below, the four images show a normal chest x-ray (top left corner), a patient with cardiomegaly (lower right corner), and a chest x-ray with a water bottle sign (lower right corner). The water bottle shape appears in the upper right corner.
Bottom Line: Increased awareness and diagnostic techniques are the primary reasons for the exponential increase in the prevalence of cardiac sarcoidosis during the last decade. More evidence is needed to determine optimal management. First-line treatment is corticosteroids; authors recommend also using immunosuppressive therapy. For either primary or secondary prevention of ventricular arrhythmias and cardiac death, implantable-cardioverter defibrillators (ICDs) should be a consideration for all patients.
Reference: Young L, Sperry BW, Hachamovitch R. Update on treatment in cardiac sarcoidosis. Curr Treat Options Cardiovasc Med. 2017 Jun.
The Bottom Line: Infective endocarditis remains a serious condition. In previous series, the clinical features, etiology, complications, and outcome have been documented in patients with IE, which resulted in most appropriate therapies, although mortality remains high in these patients. Interestingly, few investigators have described ANCA-associated IE. These authors have thus reported ANCA in 18% to 33% of patients with IE.
References: Antineutrophil Cytoplasmic Antibodies Associated With Infective Endocarditis. (n.d.). Medicine., 95(3), Medicine. , 2016, Vol.95(3).
Summary: Infection-associated ANCA may be triggered by many immune dysfunction in response to microbial peptides leading to: upregulation of autoantigen genes, molecular mimicry between pathogen microorganisms and self-antigens, formation of neutrophil extracellular traps, interaction of pathogen microorganism components with toll-like receptors. More recently, the association between infective endocarditis (IE) and formation of ANCA has also been reported
Ventricular arrhythmia (VA) in structurally normal hearts can be broadly considered under non–life-threatening monomorphic and life-threatening polymorphic rhythms. Monomorphic VA is classified on the basis of site of origin in the heart, and the most common areas are the ventricular outflow tracts and left ventricular fascicles. The morphology of the QRS complexes on electrocardiogram is an excellent tool to identify the site of origin of the rhythm.
Eric N Prystowsky Benzy J Padanilam Sandeep Joshi Richard I Fogel Ventricular arrhythmias in the absence of structural heart disease.
Journal of the American College of Cardiology , 2012, Vol.59(20), p.1733-1744
Polymorphic ventricular tachycardia (VT) is rare and generally occurs in patients with genetic ion channel disorders including long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, and short QT syndrome. Unlike monomorphic VT, these arrhythmic syndromes are associated with sudden death. While the cardiac gross morphology is normal, suggesting a structurally normal heart, abnormalities exist at the molecular level and predispose them to arrhythmias.
Table 1 Classification of Ventricular Arrhythmias in the Absence of Structural Heart Disease. : Page 1734
Bottom line: Three studies have attributed arterial thromboembolic events to cardiogenic sources in 33%, 51%, and 66% of cases. Studies of larger populations are needed.
Mural thrombus of the aorta: an important, frequently neglected cause of large peripheral emboli. G M Williams, D Harrington, J Burdick, R I White. Annals of surgery. , 1981, Vol.194(6), p.737-744.
“Large filling defects within the lumen of the aorta” were found “in 20 of 39 patients with sudden occlusion of a distal artery.” Sources of the remaining 19 occlusions were not discussed. Seven of the 20 were on heparin. “While paradoxical hypercoagulability produced by heparin is now well recognized, careful evaluation of our cases treated with heparin has not helped us to determine whether the mural thrombus was prompted by heparin or was associated with the hypercoagulable state which prompted the use of heparin.”
Paradoxical embolism: an underestimated entity. A plea for comprehensive work-up. A F AbuRahma, F C Lucente, J P Boland. Journal of cardiovascular surgery. , 1990, Vol.31(6), p.685-692.
Reviewed 41 cases of arterial embolism. Twenty-seven were attributed to cardiogenic sources. “The sources of emboli were probable cardiac (8 = 20%)…possible cardiac (12 = 29%)…probable arterio-arterial (7 = 17%)…probable paradoxical embolism (2 = 5%)…possible paradoxical embolism (3 = 7%)…and unknown source (9 = 22%).”
Etiology of peripheral arterial thromboembolism in young patients. A F AbuRahma, B K Richmond, P A Robinson. The American journal of surgery. , 1998, Vol.176(2), p.158-161.
Studied 51 patients with peripheral arterial thromboembolic events (PATE) in patients less than 50 years old over a recent 10-year period. “The sources of emboli were classified as (1) conventional (cardiac or arterioarterial), (2) unconventional, or (3) unknown…. Twenty-nine patients (57%) had unconventional causes (8 paradoxical emboli, 4 possible paradoxical emboli, 12 hypercoagulable states, 3 white clot syndromes, and 2 cervical ribs), 17 (33%) had conventional causes, and 5 (10%) were unknown.”