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Resolution of Symptomatic Intermittent Sinoatrial Exit Block Associated With Unstable Angina Following Percutaneous Coronary Intervention

ABSTRACT: Bradyarrhythmia commonly occurs because of degenerative fibrosis in the conductive system. Ischemic disease is a rare etiology and limited cases have demonstrated direct evidence of ischemia to the sinus node vessels. We report a 62-year-old Hispanic male with a significant medical history of diabetes mellitus type II (DM II), hypertension, and dyslipidemia who was admitted to our hospital for symptomatic sinoatrial (SA) exit block. Patient had no electrolyte abnormalities and our differential included ischemic vs. fibrotic or infiltrative pathologies, giving symptomatic bradycardia, cardiac chest pain, and high-risk factors for coronary artery disease. We decided to take him for cardiac catheterization which revealed sluggish, pulsatile flow into the SA nodal artery due to severe stenosis of the ostial right coronary along with sever distal left circumflex (LCX) lesion. The flow into the sinus nodal artery (SNA) markedly improved post percutaneous coronary intervention (PCI) of the right coronary artery (RCA) and distal LCX and restoration of flow into SNA. Resolution of his bradyarrhythmia and symptoms post intervention confirmed our suspicious for reversible ischemic sinus node dysfunctions. Therefore, ischemic pathologies should be thought of when other common etiologies are less likely. Coronary angiogram should be considered prior to pacemaker evaluation in these setting to avoid missing reversible causes of bradyarrhythmia.

SUBMITTER: Fadah K

PROVIDER: S-EPMC9239504 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Preinfarction angina may act as a clinical surrogate of ischemic preconditioning that may reduce infarct size and improve mortality in the setting of thrombolytic therapy for ST-elevation myocardial infarction. However, the benefits of preinfarction angina in the setting of primary percutaneous coronary intervention with stenting is inconclusive because of the greater achievement of infarct artery patency and speed of reperfusion.To identify a homogeneous population, we performed a retrospective analysis of 1031 patients admitted with a first ST-elevation myocardial infarction with ischemic times between 1 and 6 hours who received primary percutaneous coronary intervention. We identified 245 patients who had occluded arteries on presentation, of which 79 patients had documented preinfarction angina defined as chest pain within 24 hours of infarction. Infarct size was measured as the peak creatine kinase level, a metric supported in a subgroup by late enhancement on cardiac magnetic resonance imaging. Patients with preinfarction angina (n=79) had a 50% reduction in infarct size compared with those patients without preinfarction angina (n=166) by both peak creatine kinase (1094±75 IU/L versus 2270±102 IU/L; P<0.0001) and creatine kinase area under curve (18 420±18 941 versus 36 810±21 741 IU/h per liter; P<0.0001) despite having identical ischemic times (185±8 minutes versus 181±5 minutes; P=0.67) and angiographic area at risk (24.1±1.2% versus 25.3±0.9%; P=0.43). There was an absolute 4% improvement in left ventricular ejection fraction before discharge in those patients with preinfarction angina (P<0.02).The occurrence of preinfarction angina is associated with significant myocardial protection in the setting of primary percutaneous coronary intervention with stenting during ST-elevation myocardial infarction. Because preinfarction angina is relatively common, it is important that these patients be identified in clinical trials investigating therapies designed to reduce reperfusion injury and infarct size.

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Resolution of Symptomatic Intermittent Sinoatrial Exit Block Associated With Unstable Angina Following Percutaneous Coronary Intervention

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