Suspected Brugada Phenocopy Secondary to Coronary Slow Flow.
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ABSTRACT:
SUBMITTER: Shim A
PROVIDER: S-EPMC6925924 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Brugada syndrome (BrS) is an inherited disorder of cardiac ion channels characterized by peculiar ECG findings predisposing individuals to ventricular arrhythmias, syncope, and sudden cardiac death (SCD). Various electrolyte disturbances and ion channels blocking drugs could also provoke BrS ECG findings without genetic BrS. Clinical differentiation and recognition are essential for guiding the legitimate action. Hyperkalemia is well known to cause a wide variety of ECG manifestations. Severe hyperkalemia can even cause life threatening ventricular arrhythmias and cardiac conduction abnormalities. Most common ECG findings include peaked tall T waves with short PR interval and wide QRS complex. Since it is very commonly encountered disorder, physicians need to be aware of even its rare ECG manifestations, which include ST segment elevation and Brugada pattern ECG (BrP). We are adding a case to the limited literature about hyperkalemia induced reversible Brugada pattern ECG changes.
| S-EPMC5343243 | biostudies-other
Project description:BACKGROUND:Psychiatric disorders (depression / anxiety) are linked to coronary artery disease (CAD). Coronary slow flow (CSF) is a relatively common form of CAD with the same underlying mechanisms that are attributed to many anatomic and pathophysiologic factors. However, the relationship between psychiatric disorders and CSF is less well-established; and this is the aim of this study. METHODS:This cross-sectional observational study was conducted on the first 50 consecutive patients diagnosed with CSF by elective coronary angiography (CAG). They were compared with another 50 consecutive patients showing normal coronaries by CAG. Beck Anxiety Inventory and Beck Depression Inventory were used for assessment. CSF was diagnosed by coronary angiography "Thrombolysis In Myocardial Infarction" frame count. Lipid profile was obtained for all patients. RESULTS:Traditional risk factors (male gender, smoking, total cholesterol, low-density lipoproteins and triglycerides) were higher in the CSF group. Depression and anxiety scores were also higher in the CSF group. On multivariate analysis, male gender, depression and high triglycerides were the only significant independent predictors of CSF. A significant correlation existed between CSF and both anxiety and depression scores. Both scores were also significantly higher in multivessel vs single vessel affection. CONCLUSION:Psychiatric depression, male gender and high triglycerides are highly associated with CSF in patients undergoing elective CAG. There is a significant correlation between CSF severity and the severity of both anxiety and depression. Further studies are warranted to explore the impact of psychological intervention on CSF and its long-term outcome.
| S-EPMC6728014 | biostudies-literature
Project description:Brugada phenocopy (BrP) refers to a group of clinical conditions that have etiologies distinct from Brugada syndrome (BrS). Although both demonstrate features of ST-segment elevation in the right precordial leads on the electrocardiogram (ECG), one must be distinguished from the other as their treatment options are different. We report a male patient who presented with recurrent syncope with a Brugada and a S1Q3T3 pattern on the ECG. Acute pulmonary embolism (APE) complicated by BrS was suspected. Twenty-four hours Holter monitoring did not demonstrate any evidence of ventricular arrhythmias. Computed tomography pulmonary angiogram confirmed the presence of an APE. He was treated with low molecular weight heparin and a repeat ECG taken the next day showed resolution of the Brugada and S1Q3T3 patterns. This case report illustrates that APE and BrS can present with similar clinical and electrocardiographic features of recurrent syncope and Brugada pattern, respectively.
| S-EPMC5448458 | biostudies-literature
Project description:We report the case of a 55-year-old man who presented with acute coronary syndrome due to coronary slow flow after spinal cord injury. Data regarding the causes and clinical manifestations of coronary slow flow are inconclusive, but the autonomic nervous system is believed to be at least a contributing factor. The predominant vagal activity causes vasodilation and hemostasis, which can lead to acute coronary syndrome. We hereby call attention to hyperactive parasympathetic tonicity, which can lead to coronary slow flow and acute coronary syndrome in acute spinal cord injury patients.
| S-EPMC3147186 | biostudies-literature
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| S-EPMC8183737 | biostudies-literature
Project description:Pathomechanism of coronary slow flow phenomenon remains largely unclear now. Present study observed the pathological and angiographic evolution in a pig model of coronary slow flow.Coronary slow flow was induced by repeat coronary injection of small doses of 40 µm microspheres in 18 male domestic pigs and angiographic and pathological changes were determined at 3 hours, 7 days, and 28 days after microspheres injection.Compared to control group treated with coronary saline injection (n = 6) and baseline level, coronary flow was significantly reduced at 3 hours and 7 days but completely recovered at 28 days after coronary microsphere injection in slow flow group. Despite normal coronary flow at 28 days after microsphere injection, enhanced myocardial cytokine expression, left ventricular dysfunction, adverse remodelling, and ischemia/microembolism related pathological changes still persisted or even progressed from 3 hours to 28 days after coronary microsphere injection.Our results show that this large animal slow flow model could partly reflect the chronic angiographic, hemodynamic, and pathological changes of coronary slow flow and could be used to test new therapy strategies against the slow flow phenomenon.
| S-EPMC4619871 | biostudies-literature
Project description:OBJECTIVE:Coronary slow flow phenomenon (CSFP) is characterized by the decreased rate of contrast progression in epicardial coronary arteries in the absence of significant coronary stenosis. Mounting evidence has showed a significant association between inflammation and CSFP severity. This study aimed to evaluate possible associations between interleukin-1 receptor antagonist (IL-1ra) gene variable number tandem repeat (VNTR), IL-1ß -511 single nucleotide (SNP), and IL-1ß+3954 SNP mutations with CSFP. METHODS:Forty-eight patients with CSFP and 62 controls with angiographically normal coronary arteries were prospectively enrolled in the study. Genotypes were assessed using the polymerase chain reaction (PCR)-based restriction fragment length polymorphism (PCR-RFLP) technique. RESULTS:Homozygote genotype for allele 2 of+3954 C>T 2/2 genotype was significantly more frequent in patients with CSFP than in the control group, whereas 1/2 genotype was more frequent in the control group (35.4% versus 14.5% for 2/2 genotype and 25% versus 35.5% for 1/2 genotype in CSFP and control groups, respectively, X2=6.6; p=0.04). The allelic frequency of allele 2 of this polymorphism was significantly higher in the CSFP group than in the control group (47.9% versus 28.6% in the control group, X2=5.6; p=0.02). However, there was no significant difference with regard to genotype or allelic frequencies of IL-1ra VNTR or IL-1ß -511 SNP polymorphisms between patients with CSFP and controls. CONCLUSION:IL-1ß+3954 SNP mutations are significantly more common in patients with CSFP. It may suggest that the tendency for inflammation may contribute to the presence of this phenomenon.
| S-EPMC5864788 | biostudies-literature
Project description:Background: In recent years, Wolff-Parkinson-White (WPW) syndrome and Brugada electrocardiogram (ECG) patterns have been reported as coexistent in the same patient. In most cases, the two waveforms appeared separately. Here, we described combinations of different waveforms on one ECG, such as the Brugada pattern with delta waves and the Brugada pattern with paroxysmal supraventricular tachycardia (PSVT). Importantly, we recorded an alternate conversion of these combined ECG waveforms, which has not previously been reported in the literature. At the same time, we confirmed that the change in the waveform was related to fever by analyzing Holter data. Case: A 48-year-old male was admitted to our hospital due to palpitations and fever. The patient had a history of a cold 3 days ago. Laboratory examinations showed an elevated neutrophil percentage (85%) and troponin I level (0.86 ng/ml). A chest computed tomography (CT) scan showed inflammation in the right lung. The diagnosis of pneumonia and myocarditis was made. ECG indicated WPW syndrome and the Brugada pattern. We recorded the dynamic changes in this combination of delta waves and Brugada waves with a Holter monitor, and we found the changes would happen when the patient's body temperature rose. The doctors thought that the patient's pulmonary infection led to fever, which caused the changes in waveform. After treatment with antibacterial therapy and supportive care, his body temperature returned to normal. The various laboratory indicators also gradually returned to normal. The doctor recommended that the patient undergo further pre-excitation bypass radiofrequency ablation treatment, but the patient refused and was discharged. Conclusion: Delta waves and Brugada ECG patterns could appear on one ECG at the same time. There were dynamic changes of QRS complex, relating to fever.
| S-EPMC8566699 | biostudies-literature
Project description:Background Guidelines recommend that coronary slow flow phenomenon (CSFP), defined as corrected thrombolysis in myocardial infarction frame count (CTFC) >$$ > $$27, can diagnose coronary microvascular dysfunction (CMD) in patients with angina and nonobstructed coronary arteries. CSFP has also historically been regarded as a sign of coronary endothelial dysfunction (CED). We sought to validate the utility of CTFC, as a binary classifier of CSFP and as a continuous variable, to diagnose CMD and CED. Methods and Results Patients with angina and nonobstructed coronary arteries had simultaneous coronary pressure and flow velocity measured using a dual sensor-tipped guidewire during rest, adenosine-mediated hyperemia, and intracoronary acetylcholine infusion. CMD was defined as the inability to augment coronary blood flow in response to adenosine (coronary flow reserve <2.5) and CED in response to acetylcholine (acetylcholine flow reserve ≤1.5); 152 patients underwent assessment using adenosine, of whom 82 underwent further acetylcholine testing. Forty-six patients (30%) had CSFP, associated with lower flow velocity and higher microvascular resistance as compared with controls (16.5±$$ \pm $$6.9 versus 20.2±$$ \pm $$6.9 cm/s; P=0.001 and 6.26±$$ \pm $$1.83 versus 5.36±$$ \pm $$1.83 mm Hg/cm/s; P=0.009, respectively). However, as a diagnostic test, CSFP had poor sensitivity and specificity for both CMD (26.7% and 65.2%) and CED (21.1% and 56.0%). Furthermore, on receiver operating characteristics analyses, CTFC could not predict CMD or CED (area under the curve, 0.41 [95% CI, 0.32%-0.50%] and 0.36 [95% CI, 0.23%-0.49%], respectively). Conclusions In patients with angina and nonobstructed coronary arteries, CSFP and CTFC are not diagnostic of CMD or CED. Guidelines supporting the use of CTFC in the diagnosis of CMD should be revisited.
| S-EPMC9973578 | biostudies-literature
Project description:To investigate intercellular adhesion molecule-1 (ICAM1) and angiotensinogen (AGT) gene polymorphisms, as related to atherosclerosis and endothelial dysfunction, in coronary slow flow (CSF).The participants in this study were 48 patients with CSF and 67 patients with normal coronary flow as controls. The K469E polymorphism of ICAM1 (rs5498) and the T207M polymorphism of AGT (rs4762) were determined using the polymerase chain reaction amplification method.Baseline demographic parameters were similar in both groups. The mean thrombolysis in myocardial infarction frame count was significantly higher in patients with CSF (23.8 ± 5.1) compared to the controls (13.3 ± 2.6, p < 0.001). A significant association was found between the ICAM1 K allele and CSF (OR: 1.96, 95% CI: 1.15-3.35, p = 0.013). There was no difference in the frequency of AGT T207M genotypes in the patients with CSF and the control subjects.This study showed that K469E polymorphisms of ICAM1 that play a role in atherosclerotic pathogenesis are related to CSF.
| S-EPMC5586901 | biostudies-literature