C oronary artery phasic compression can be caused by spasm or myocardial bridging, or by acquired anatomic changes to the surrounding heart chambers that exert mechanical pressure in conjunction with contractility. Treatment varies in accordance with cause; therefore, recognizing and understanding this phenomenon is important. We report here the case of a symptomatic patient in whom we found phasic coronary artery compression, and we discuss the few published, relevant reports. Case ReportIn September 2013, a 55-year-old obese black man (body mass index, 43.5 kg/m 2 ) presented with exertional dyspnea that had worsened over several months. He had multiple cardiac risk factors, including uncontrolled hypertension and a distant history of alcohol abuse. He reported orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema, but no fever, chills, chest pain, nausea, vomiting, or recent illness. His blood pressure upon presentation was 145/85 mmHg. A chest radiograph showed cardiomegaly and bilateral pulmonary congestion. He had a mildly elevated pro-brain natriuretic peptide level, and test results for cardiac troponins were negative.An electrocardiogram (ECG) revealed an ectopic atrial rhythm that indicated left atrial enlargement (Fig. 1). A transthoracic echocardiogram showed an enlarged left ventricle (LV) with severe global hypokinesis, and marked left atrial dilation (Fig. 2). The patient's LV ejection fraction was low (0.15-0.20). Grade III diastolic dysfunction and elevated left atrial filling pressure were also seen.A coronary angiogram showed a left-dominant system with nonobstructive coronary artery disease. The LV end-diastolic pressure was elevated (33 mmHg) and decreased only minimally when intraventricular nitroglycerin was administered, further correlating with chronically elevated left atrial pressure.
Patient: Male, 41Final Diagnosis: Sick Sinus Syndrome and absent left main coronary artery • separate ostia of left anterior descending and circumflex arteries in Holt-Oram SyndromeSymptoms: Conduction disturbance • seizure-like activity • upper extremity malformationsMedication: —Clinical Procedure: Electro physiology study • coronary catheterization • pacemakerSpecialty: CardiologyObjective:Congenital defects/diseasesBackground:Holt-Oram syndrome (HOS) is a rare but significant syndrome consisting of structural heart defects, conduction abnormalities, and upper extremity anomalies. It was first described in the British Heart Journal in 1960 by Mary Holt and Samuel Oram as a report of atrial septal defect, conduction disturbances, and hand malformations occurring in family members. Patients can present with heart blocks or symptoms of underlying congenital heart defects.Case Report:A 41-year-old man with Holt-Oram syndrome presented with seizure-like activity and was found to have an underlying conduction disturbance. Physical exam showed bilateral atrophic upper extremities with anatomic disfiguration, and weakness of the intrinsic hand muscles. Cardiovascular exam revealed a slow heart rate with irregular rhythm. EKG showed sinus arrest with junctional escape rhythm. Cardiac catheterization revealed coronary anomalies, including absent left main coronary artery and separate ostia of the left anterior ascending and left circumflex coronary artery. Coronary arteries were patent. Following electrophysiology study, sick sinus syndrome and AV block were diagnosed, and the patient received implantation of a permanent pacemaker.Conclusions:This patient presented with a seizure-like episode attributed to hypoxia during asystole from an underlying cardiac conduction defect associated with Holt-Oram syndrome. Arrhythmias and heart blocks are seen in these patients, and conduction defects are highly associated with congenital heart defects. Holt-Oram syndrome rarely presents with coronary artery anomalies. There is no reported case of separate coronary ostia and absent left main coronary artery. Prompt diagnosis is important since anomalies in coronary and upper extremity vasculature might be challenging for invasive procedures.
Electromagnetic interference (EMI) includes any electromagnetic field signal that can be detected by device circuitry, with potentially serious consequences: incorrect sensing, pacing, device mode switching, and defibrillation. This is a unique case of extracardiac EMI by alternating current leakage from a submerged motor used to recycle chlorinated water, resulting in false rhythm detection and inappropriate ICD discharge. A 31-year-old female with arrhythmogenic right ventricular cardiomyopathy and Medtronic dual-chamber ICD placement presented after several inappropriate ICD shocks at the public swimming pool. Patient had never received prior shocks and device was appropriate at all regular follow-ups. Intracardiac electrograms revealed unique, high-frequency signals at exactly 120 msec suggestive of EMI from a strong external source of alternating current. Electrical artifact was incorrectly sensed as a ventricular arrhythmia which resulted in discharge. ICD parameters including sensing, pacing thresholds, and impedance were all normal suggesting against device malfunction. With device failure and intracardiac sources excluded, EMI was therefore strongly suspected. Avoidance of EMI source brought complete resolution with no further inappropriate shocks. After exclusion of intracardiac interference, device malfunction, and abnormal settings, extracardiac etiologies such as EMI must be thoughtfully considered and excluded. Elimination of inappropriate shocks is to “first, do no harm.”
Radiofrequency (RF) ablation is the first-line management of cavo-tricuspid isthmus dependent atrial flutter. It has been performed with 95% success rate. Adverse events are very rare. We report the first case of acute severe mitral regurgitation (MR) and complete heart block developed after successful atrial flutter ablation. A 62-year-old female with mild MR presented with palpitations. Surface electrocardiogram was suggestive of isthmus dependent atrial flutter. A duodecapolar mapping catheter showed an atrial flutter with cycle length of 280 ms. An 8 mm tipped Thermistor RF ablation catheter was placed at the cavo-tricuspid isthmus. RF energy was delivered as the catheter was dragged to the inferior vena cava. Temperature limit was 60 °C; the power output limit was 60 W. The patient converted to sinus rhythm with the first ablation line. Bi-directional block was recorded. Two additional ablation lines lasting 60 - 120 s were delivered. The patient started having chest pain and developed complete heart block with no escape rhythm. She became hypotensive and was immediately paced from the right ventricle. There were no signs of pericardial tamponade. Emergent bedside echo demonstrated severe MR with a retracted posteromedial mitral valve leaflet. She was 100% paced and EKG changes could not be assessed. Based on the sudden onset chest pain, hypotension, complete heart block and acute severe MR after ablation, the right coronary artery occlusion was suspected. She was immediately transferred to the catheterization laboratory. Coronary angiography revealed a total occlusion of the posterolateral branch from the right coronary artery. Balloon angioplasty and coronary artery stenting was performed. Complete heart block subsequently resolved. Subsequent bedside echocardiogram showed marked improvement of the MR. Patients with smaller body size have smaller hearts and more likely to have injury from RF current. Higher energy penetrates deeper and causes more tissue damage. The use of lower temperature limits (55 °C) and lower energy (60 W) for small, elderly, and female patients is encouraged.
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