Tachyarrhythmias, bradyarrhythmias and acute coronary syndromes

Trappe, Hans‐Joachim

doi:10.4103/0974-2700.62112

Cited by 11 publications

(9 citation statements)

References 26 publications

(23 reference statements)

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“…Electrical conduction abnormalities are well-recognized complications of acute myocardial infarction. 6 They are caused by either autonomic imbalance or ischemia and subsequent necrosis of the conduction system. The most common clinical presentation is bradycardia, which may or may not be symptomatic.…”

Section: Discussionmentioning

confidence: 99%

Severe Bradycardia Prior to Coronary Artery Bypass Graft Surgery: A Case Report

Harky

Bashir

Grafton-Clarke

et al. 2018

JTHC

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Intraventricular conduction abnormalities following cardiac surgery have been thoroughly described, especially after valvular surgery. It is also widely known that several anesthetic factors can cause autonomic disturbances resulting in the unmasking of sinus node dysfunction, significant bradycardia, and cardiovascular collapse during the intraoperative period. However, little is known about asymptomatic episodes, especially those occurring prior to coronary artery bypass grafting (CABG). We report a rare occurrence of an intraventricular conduction defect that presented in an asymptomatic patient following non–ST-elevation myocardial infarction prior to urgent CABG. Our patient presented with sudden-onset chest pain, and following coronary angiography he was found to have triple-vessel coronary disease. During anesthetic induction for inpatient CABG surgery, he developed episodes of acute sinus tachy-brady episodes, requiring a stat dose of adrenaline to maintain the heart rate prior to the establishment of cardiopulmonary bypass. The arrhythmia persisted postoperatively, necessitating the insertion of a permanent dual-chamber pacemaker for complete heart block. The patient was later discharged without further complications, and upon follow-up 12 months later, he remains in good health.

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Section: Discussionmentioning

confidence: 99%

Severe Bradycardia Prior to Coronary Artery Bypass Graft Surgery: A Case Report

Harky

Bashir

Grafton-Clarke

et al. 2018

JTHC

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“…The exact mechanism associated to the decrease in heart rate in MI animals remains unclear. A possible explanation could be the presence of bradyarrhythmia associated with atrioventricular (AV) block (subsequent to AV node ischaemia), which may be persistent in anterior MI (Trappe, ). It is enticing to speculate that MAG treatment prevented extensive ischaemia and the development of bradycardia.…”

Section: Discussionmentioning

confidence: 99%

Post-ischaemic angiogenic therapy usingin vivoprevascularized ascorbic acid-enriched myocardial artificial grafts improves heart function in a rat model

Martinez

Wang

Lilyanna

et al. 2011

J Tissue Eng Regen Med

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Angiogenesis plays a key role in post-ischaemic myocardial repair. We hypothesized that epicardial implantation of an ascorbic acid (AA)-enriched myocardial artificial graft (MAG), which has been prevascularized in the recipients' own body, promotes restoration of the ischaemic heart. Gelatin patches were seeded with GFP-luciferase-expressing rat cardiomyoblasts and enriched with 5 μm AA. Grafts were prevascularized in vivo for 3 days, using a renal pouch model in rats. The MAG patch was then implanted into the same rat's ischaemic heart following myocardial infarction (MI). MAG-treated animals (MAG group, n = 6) were compared to untreated infarcted animals as injury controls (MI group, n = 6) and sham-operated rats as healthy controls (healthy group, n = 7). In vivo bioluminescence imaging indicated a decrease in donor cell survival by 83% during the first week post-implantation. Echocardiographic and haemodynamic assessment 4 weeks after MI revealed that MAG treatment attenuated left ventricular (LV) remodelling (LV end-systolic volume, 0.31 ± 0.13 vs 0.81 ± 0.01 ml, p < 0.05; LV end-diastolic volume 0.79 ± 0.33 vs 1.83 ± 0.26 ml, p < 0.076) and preserved LV wall thickness (0.21 ± 0.03 vs 0.09 ± 0.005 cm, p < 0.05) compared to the MI group. Cardiac output was higher in MAG than MI (51.59 ± 6.5 vs 25.06 ± 4.24 ml/min, p < 0.01) and comparable to healthy rats (47.08 ± 1.9 ml/min). Histology showed decreased fibrosis, and a seven-fold increase in blood vessel density in the scar area of MAG compared to MI group (15.3 ± 1.1 vs 2.1 ± 0.3 blood vessels/hpf, p < 0.0001). Implantation of AA-enriched prevascularized grafts enhanced vascularity in ischaemic rat hearts, attenuated LV remodelling and preserved LV function.

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“…Bradycardia may also be a presentation of infarct to the sinoatrial region of the myocardium. 3 Therefore, it is essential to obtain cardiac biomarkers to further investigate. Atenolol overdose and hyperkalemia See end of article for correct answers to questions.…”

Section: Based On This Patient's History and Phys-mentioning

confidence: 99%

66-Year-Old Man With Light-headedness, Chest Pain, and Dyspnea

Clark

Fuente

Hafdahl

2019

Mayo Clinic Proceedings

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A 66-year-old white man with a medical history of chronic kidney disease (CKD) stage 3a (baseline creatinine level of 1.4 mg/dL; normal 0.74-1.35 mg/dL) with an estimated glomerular filtration rate of 52 mL/min per 1.73 m 2 per the Chronic Kidney Disease Epidemiology collaboration equation, controlled type 2 diabetes mellitus with microalbuminuria, hypertension, hyperlipidemia, and medically complicated obesity (body mass index, 37) presented to his primary care clinic with episodes of orthostatic light-headedness that had been occurring for approximately 2 weeks. These episodes were also associated with chest tightness and dyspnea. Symptoms occurred only while standing or ambulating and never while at rest. He reported no palpitations, vertiginous symptoms, recent fevers or chills, hemoptysis, known sick contacts, or insect bite exposures. His lightheadedness, chest pain, and dyspnea worsened on the day before presentation, prompting a visit to his physician for further evaluation. He reported that he had been taking his blood pressure medications including amlodipine, lisinopril, atenolol, and spironolactonehydrochlorothiazide, as well as his other medications (metformin, aspirin, and pravastatin) regularly and as instructed. He had noted a considerable decrease in his urine output over the previous day. He had no recent travel, surgical procedures, immobilization, history of pulmonary embolism (PE), deep venous thrombosis, or active malignancy.On physical examination, he appeared nontoxic but had bradycardia (heart rate, 25 beats/min) with hypotension (blood pressure, 90/40 mm Hg) and a respiratory rate of 14 breaths/min. No rashes, lymphadenopathy, or peripheral edema were noted. Heart examination revealed no murmurs, and lung examination findings were normal. He was alert and in no distress. Results of abdominal examination and the remainder of the neurologic examination were unremarkable. Given his severe symptomatic bradycardia and borderline hypotension, he was referred to the emergency department (ED) for further evaluation.

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Tachyarrhythmias, bradyarrhythmias and acute coronary syndromes

Cited by 11 publications

References 26 publications

Severe Bradycardia Prior to Coronary Artery Bypass Graft Surgery: A Case Report

Severe Bradycardia Prior to Coronary Artery Bypass Graft Surgery: A Case Report

Post-ischaemic angiogenic therapy usingin vivoprevascularized ascorbic acid-enriched myocardial artificial grafts improves heart function in a rat model

66-Year-Old Man With Light-headedness, Chest Pain, and Dyspnea

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