A Patient With Athlete’s Heart Syndrome: When the Abnormal Is Normal
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Long-term athletic training can result in structural and conduction changes within the heart, leading to Athlete's heart syndrome (AHS). This syndrome is characterized by increased left ventricle (LV) dimensions, thickness, and mass. Dynamic exercise significantly contributes to these alterations, with sinus bradycardia being a common conduction abnormality, often accompanied by first-degree atrioventricular (AV) block. However, higher degrees of AV conduction abnormalities, such as second- and third-degree blocks, though rare, might occur due to parasympathetic hypertonia. Prompt evaluation is necessary to rule out underlying structural or infiltrative heart diseases. We present the case of a 66-year-old lifelong long-distance runner with marked sinus bradycardia, AV dissociation, and junctional escape rhythm, alongside left ventricular hypertrophy (LVH) and T-wave repolarization abnormalities. Subsequent studies ruled out possible pathologies, and the patient was diagnosed with AHS, characterized by cardiac remodeling and bradycardia due to prolonged cardiac loading. This case underscores the importance of clinical assessment, cardiac imaging, and exclusion of pathologic causes to distinguish normal physiological adaptations from potentially concerning conditions.Keywords:
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Remdesivir has been extensively employed during the coronavirus disease 2019 (COVID-19) pandemic as it has proven to be efficacious against the causative SARS-CoV-2. However, there is not much evidence on the cardiovascular adverse effect profile of remdesivir. In addition, limited data support the occurrence of sinus bradycardia associated with remdesivir. Herein we chronicle a clinical encounter of a patient suffering from COVID-19 whose clinical course was complicated by marked sinus bradycardia that began acutely after remdesivir initiation and resolved on cessation of the medication. The patient denied symptoms and completed a 5-day course with a resolution of bradycardia on completion of medication. We suggest that the physicians be cognizant of this rare side effect of remdesivir and suggest a continuation of this medication unless symptomatic bradycardia precludes management.
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SARS COV-2 infection has become a global threat. Cardiovascular manifestations associated with Covid-19 have been noted in several publications, and bradycardia related to Covid-19 is a commonly reported complication. This study reports six serial cases of bradycardia attributable to Covid-19; four of them developed complete atrioventricular block. These patients experienced clinical symptoms related to bradycardia and initially required permanent pacemaker implantation. However, one patient did not require permanent pacing later on due to spontaneous conversion to sinus rhythm. In comparison, the other two patients who developed transient sinus bradycardia experienced a self-limiting condition during their hospitalization period without requiring any cardiac pacing device or medication to increase heart rate. Complete atrioventricular block and transient sinus bradycardia in these patients, despite not having any history of bradycardia, might be due to complex processes in the systemic inflammatory response in Covid-19. Cardiac monitoring, hemodynamic evaluation, and strategy for permanent pacemaker in these patients should be treated on a case-by-case basis.
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We present a case of a 54-year-old woman with asymptomatic bradycardia who was referred for consideration of a pacemaker for profound chronic sinus bradycardia (heart rate is 33 beats per minute). Further, history and physical revealed a self-described endurance athlete with severe anorexia nervosa (AN). Background. Anorexia nervosa and endurance training are known contributors to bradycardia; however, profound asymptomatic sinus bradycardia in the 20-30 beats per minute is underdocumented in the literature and not a common presentation in any setting. The decision to implant a permanent pacemaker could potentially lead to further physical and psychological repercussions in such a frail patient.
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We examined the relationship between postpacing T wave changes and monophasic action potentials recorded from the ventricle in dogs. MAPs were recorded from the right and left ventricle before and after cessation of pacing. The duration of the MAP was calculated as the time in milliseconds from the upstroke to 90% repolarization (MAPD90). T waves in limb leads were flat or had a biphasic pattern, eventually becoming negative after pacing. The Q-T interval of the escape beat after pacing was prolonged compared with the control. After right ventricular pacing, the average duration of MAPD90 in the right ventricle, but not in the left ventricle, was prolonged. (right MAPD: control 275 +/- 10 ms; after pacing: 311 +/- 17 ms, p < 0.05; left MAPD: control: 266 +/- 23 ms, after pacing: 284 +/- 26 ms, NS). After left ventricular pacing, the average duration of MAPD90 in the left ventricle, but not in the right ventricle, was prolonged (right MAPD: control: 247 +/- 75 ms, after pacing: 287 +/- 39 ms, NS; left MAPD: control: 257 +/- 23 ms, after pacing: 303 +/- 25 ms, p < 0.05). Furthermore, the average duration of MAPD90 at the pacing site became progressively prolonged over time. These results suggest that myocardial cells retain the memory of abnormal repolarization associated with pacing.
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Bradycardia was documented in 12 cattle from which food has been withheld for 48 hours in preparation for general anesthesia and an elective surgical procedure. The heart rates decreased by a mean of 14 beats/min, and 4 cows had sinus arrhythmia. To evaluate this finding, the heart rates of 21 clinically normal cattle were evaluated before and after food was withheld for 48 hours. Bradycardia developed in all of the clinically normal cattle, with the mean decrease in heart rate being 23 beats/min. Five of the clinically normal cows developed sinus arrhythmia. It was concluded that bradycardia and sinus arrhythmia in cattle are associated with deprivation of food.
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Steroids are one of the most commonly used drugs and known to be associated with several side effects. There have been case reports about the associated sinus bradycardia with pulse dose corticosteroids administration both IV and oral. We present a case of asymptomatic sinus bradycardia associated with oral prednisone 40 mg. A 69-year-old male was admitted to the ICU for sepsis and subsequently was found to have gastrointestinal (GI) bleed. He developed an acute gout attack during hospitalization and was treated with prednisone 40 mg. Over the next 24 hours, the patient's heart rate dropped to 30s to 40s beats/minute while other vitals have remained stable. He was monitored on telemetry and review of the rhythm strips, as well as a 12-lead electrocardiogram (EKG), that showed sinus bradycardia; no pauses or atrio-ventricular (AV) nodal blocks were identified. The patient was not on any beta blocker or other therapies commonly associated with sinus bradycardia. His steroids were stopped while all other medications were continued. His heart rate slowly started to improve over the next 24 hours. He was not found to have any further episodes of bradycardia. Our case is unusual as we noted transient asymptomatic bradycardia with oral prednisone 40 mg dose. While bradycardia is reversible and may go unnoticed, it is important for the clinician to be aware of this adverse effect and include it in the list of potential differentials for bradycardia.
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This chapter covers bradycardia, heart blocks, and cardiac pacing. Bradyarrhythmias that require pacing can be caused by a range of aetiologies and early identification of possible reversible causes is the first stage of treatment. Although a degree of bradycardia and heart blocks might not have any clinical significance, it is always important to assess the patient for signs of adverse effects. Generally, pacing is only indicated for symptomatic sinus bradycardia. In contrast, patients with asymptomatic atrioventricular block may require pacing for prognostic purposes.
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High dose corticosteroid therapy is widely used as attack therapy of inflammatory central nervous system disorders and can induce several adverse reactions. Bradycardia is an infrequent event after corticosteroids administration and is often asymptomatic. We report a case of a woman admitted to the neurological department of our hospital for paraesthesias of the lower limbs. She received adiagnosis of inflammatory myelitis and high dose corticosteroid therapy was prescribed. During the therapy she complained of chest tightness, dyspnoea, weakness and malaise. An electrocardiogram revealed sinus bradycardia. A significant increase in body weight, probably due to plasma volume expansion, was detected. Bradycardia and high blood pressure spontaneously resolved in few days. We provide a collection and a statistical analysis of literature data about steroid induced bradycardia. We found that higher total doses are associated with lower pulse rate and symptomatic bradycardia. Bradycardia is more frequent in older patients and those with underlying cardiac disease or with autonomic disturbance. However clinicians must be aware about the occurrence of symptomatic bradycardia in all patients who undergo high dose corticosteroid therapy, not only in those at risk, to early detect and treat this potentially dangerous condition.
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