Is ischemic stimulus involved for J wave augmentation during coronary angiography and intracoronary administration of normal saline?

BACKGROUND: J waves may be augmented by coronary angiography (CAG) or intracoronary drug administration but the underlying mechanism is unknown. PURPOSE: The effect of intracoronary normal saline (NS) on J waves were investigated. PATIENTS AND METHODS: After the standard CAG using iopamidol (IopamiroR Inj), NS was injected into the right coronary artery in 10 patients with and eight patients without J waves at the baseline. The 12-lead ECG was monitored, stored on a computer and retrieved later for measurement of the J wave amplitude before or during the coronary interventions. RESULTS: J waves in leads II, III and aVF at baseline increased significantly in each lead during the right CAG and NS injection into the right coronary artery. The J wave changes were similar between the two interventions and distinct similar alterations were observed in the QRS complex. We postulated that the ischemic myocardium that was induced during CAG or intracoronary NS administration slowed the conduction velocity of depolarization in the perfusion territory and delayed the timing of J waves to appear. Then, the delayed appearance of J waves would be less opposed by electromotive force from other areas resulting in augmentation. CONCLUSION: J wave augmentation was observed during CAG and intracoronary NS administration. As a mechanism of augmentation, we postulated that contrast media and NS induce myocardial ischemia and delay the timing of J waves to a point of less opposition by electromotive force from other areas. HIGHLIGHTS: J wave augmentation has been reported during intracoronary injection of contrast media or drugs. The present study confirmed that normal saline alone was able to augment J waves. Mechanistically, coronary interventions using anoxic solutions can cause regional myocardial ischemia and reduce the conduction velocity of depolarization. Then, delayed J waves are less opposed by the electromotive force from remote areas which leads to augmentation. When a drug is diluted in normal saline and given intracoronarily, changes in J waves can be due to normal saline. The pathophysiological and clinical significance of J waves augmented during coronary interventions need to be established.

The prognostic value of J-wave pattern for recurrence of ventricular tachycardia after catheter ablation in patients with myocardial infarction.

BACKGROUND: J-waves and fragmented QRS (fQRS) on surface ECGs have been associated with the occurrence of ventricular tachyarrhythmias. Whether these non-invasive parameters can also predict ventricular tachycardia (VT) recurrence after radiofrequency catheter ablation (RFCA) is unknown. Of interest, patients with a wide QRS-complex have been excluded from clinical studies on J-waves, although a J-wave like pattern has been described for wide QRS. METHODS: We retrospectively included 168 patients (67 ± 10 years; 146 men) who underwent RFCA of post-infarct VT. J-wave pattern were defined as J-point elevation ≥ 0.1 mV in at least two leads irrespective of QRS width. fQRS was defined as various RSR` pattern in patients with narrow QRS and more than two R wave in those with wide QRS. The primary endpoint was VT recurrence after RFCA up to 24 months. RESULTS: J-wave pattern and fQRS were present in 27 and 28 patients, respectively. Overlap of J-wave pattern and fQRS was observed in nine. During a median follow-up of 20 (interquartile range 9-24) months, 46 (27%) patients had VT recurrence. Kaplan-Meier curves revealed that both J-wave pattern and fQRS were associated with VT recurrence. Multivariate Cox regression analysis demonstrated that the presence of J-wave pattern (hazard ratio [HR] 2.84; 95% confidence interval [CI] 1.45-5.58; P = .002) and greater number of induced VT (HR 1.29; 95% CI 1.15-1.45; P < .001) were the independent predictors of VT recurrence. CONCLUSIONS: A J-wave pattern-but not fQRS-is independently associated with an increased risk of post-infarct VT recurrence after RFCA irrespective of QRS width. This simple non-invasive parameter may identify patients who require additional treatment.

J waves induced during coronary angiography in patients with vasospastic angina and its implication.

BACKGROUND: J waves may develop during coronary angiography (CAG). PATIENTS AND RESULTS: Seven patients (61±6 years, 6 male) had vasospastic angina. ST-segment elevation and ventricular fibrillation were documented in all patients. CAG revealed normal arteries, but slurring or notching (J waves) with an amplitude of 0.20±0.06 mV appeared for the first time (n=6) or in an augmented manner (n=1) with distinct alterations in QRS morphology when contrast medium was injected into the right coronary artery. CONCLUSION: In patients with vasospastic angina, J waves observed during CAG can be a manifestation of a local conduction delay caused by contrast medium-induced myocardial ischemia.

A Case of J Wave Syndrome Due to Severe Hypercalcemia with Ventricular Fibrillation Storm and Successful Treatment of Isoproterenol Infusion.

A case of J wave syndrome with ventricular fibrillation (VF) storm and severe hypercalcemia due to primary hyperparathyroidism is presented. VF storm subsided with an isoproterenol infusion. Prominent J waves and a Brugada-like electrocardiogram pattern disappeared after parathyroidectomy. Ventricular tachyarrhythmia was not induced during an electrophysiological study. The patient remained asymptomatic up to the 12-month follow-up.

When the factory shuts down.

CLINICAL INTRODUCTION: A 56-year-old man without known medical history was brought to our ED after he was found next to his bed, agitated and with waxing and waning consciousness. He has been bedbound for 5 days after a long-standing period of malnutrition. Physical examination reveals Kussmaul breathing, heart rate of 62/min and blood pressure of 135/100 mm Hg, normal cardiac, abdominal and a non-focal neurological examination other than confusion and altered level of consciousness. An EKG was performed (figure 1).emermed;36/1/51/F1F1F1Figure 1EKG at presentation in our ED. QUESTION: What abnormalities are the clues to the severity of his condition? How would you confirm your suspicion?The minimally prolonged QTc time.The subtle horizontal ST segment elevation in V2 and V3.The subtle positive deflection at the J point.Nothing, this EKG is not interpretable because of the movement of baseline.

Variants of Brugada Syndrome and Early Repolarization Syndrome: An Expanded Concept of J-Wave Syndrome.

BACKGROUND: The role of J-waves in the pathogenesis of ventricular fibrillation (VF) occurring in structurally normal hearts is important. METHODS: We evaluated 127 patients who received an implantable cardioverter-defibrillator (ICD) for Brugada syndrome (BS, n = 53), early repolarization syndrome (ERS, n = 24), and patients with unknown or deferred diagnosis (n = 50). Electrocardiography (ECG), clinical characteristics, and ICD data were analyzed. RESULTS: J-waves were found in 27/50 patients with VF of unknown/deferred diagnosis. The J-waves were reminiscent of those seen in BS or ERS, and this subgroup of patients was termed variants of ERS and BS (VEB). In 12 VEB patients, the J/ST/T-wave morphology was coved, although amplitudes were <0.2 mV. In 15 patients, noncoved-type J/ST/T-waves were present in the right precordial leads. In the remaining 23 patients, no J-waves were identified. VEB patients exhibited clinical characteristics similar to those of BS and ERS patients. Phenotypic transition and overlap were observed among patients with BS, ERS, and VEB. Twelve patients with BS had background inferolateral ER, while five ERS patients showed prominent right precordial J-waves. Patients with this transient phenotype overlap showed a significantly lower shock-free survival than the rest of the study patients. CONCLUSIONS: VEB patients demonstrate ECG phenotype similar to but distinct from those of BS and ERS. The spectral nature of J-wave morphology/distribution and phenotypic transition/overlap suggest a common pathophysiologic background in patients with VEB, BS, and ERS. Prognostic implication of these ECG variations requires further investigation.

Epicardial Brugada syndrome ablation unmasking inferior J waves.

Patients with Brugada syndrome are at risk of life-threatening ventricular arrhythmias. Epicardial substrate ablation for Brugada syndrome has been described as a means of controlling these arrhythmias and recent reports describe elimination of the Brugada phenotype with ablation. We describe a unique case in which a patient developed inferior J waves with an early repolarization-type electrocardiogram following successful epicardial infundibular substrate ablation (which eliminated the Brugada syndrome electrocardiogram on ajmaline challenge). We discuss the likely underlying pathophysiology responsible for this phenomenon, its relationship to the anatomic obstacles encountered during epicardial ablation, and the implications for long-term arrhythmic risk.

Clinical Significance of J Waves in Patients Undergoing Therapeutic Hypothermia for Out-of-Hospital Cardiac Arrest.

BACKGROUND: Hypothermia is associated with the development of J waves. However, little is known about the impact of these electrocardiogram (ECG) findings on the development of ventricular arrhythmias and patient outcomes during therapeutic hypothermia (TH) postresuscitation from out-of-hospital cardiac arrest (OHCA). We investigated the prevalence of J waves in OHCA patients prior to and during TH. Additionally, we explored the incidence of atrial and ventricular arrhythmias and in-hospital mortality for patients with and without J waves either at baseline, during TH, or both. METHODS: We conducted a retrospective analysis of patients who suffered OHCA and underwent TH (goal temperature of 32-34°C). Fifty-nine patients were stratified dependent upon the presence of or the development of J waves on surface ECGs. Descriptive analysis and logistic regression modeling were used to assess the population differences and mortality, respectively, between patients who developed J waves during TH and those who did not. RESULTS: There was no difference in the development of in-hospital atrial or ventricular arrhythmias between patients with J waves present during TH (16%) and those without (17.6%, P = 0.834). Compared to patients without J waves at baseline and during TH, those with J waves present both at baseline and during TH had significantly worse survival (hazard ratio = 12.42, P = 0.046). CONCLUSIONS: While J waves are common ECG findings during TH in patients resuscitated from OHCA, our study demonstrated an increase in mortality for patients with J waves present both at baseline and during TH.

The relationship between J waves and contact of lung cancer with the heart.

BACKGROUND: J waves result mainly from an increased density of transient outward current (Ito ). Mechanical stretch to the heart activates multiple signal transduction pathways, in which Ito may be involved. The purpose of this study was to test the hypothesis that mechanical contact of lung cancer with the heart may manifest J waves. METHODS: We reviewed 12-lead electrocardiograms to examine whether J waves were associated with contact of lung cancer with the heart. J waves were defied as an elevation of ≥0.1 mV at the junction between QRS complex and ST segment with either notching or slurring morphology. The locational interaction between lung cancer and the heart was determined by computed tomography image. RESULTS: A total of 264 patients (176 men; mean 68.5 ± 10.7 years) with lung cancer were evaluated. The prevalence of J waves was 25.4% in the total population. J waves were present in 40 of 44 (90.9%) patients with the contact. In contrast, J waves were present in 25 of 220 (11.4%) patients without the contact. The sensitivity and specificity of the contact for J waves were 90.9% and 88.6%, respectively. The odds ratio of the contact with the heart to the presence of J waves was 78 (95% confidence interval 25.7-236.4). The appearance of J waves that coincided with the development of lung cancer was observed in 12 patients. CONCLUSION: The presence of J waves was associated with the contact of lung cancer with the heart.

Massive J-waves in the context of intracranial hemorrhage.

Transient ST-segment elevation may be caused by conditions other than myocardial ischemia, among them intracranial hemorrhage. Recognition of the underlying etiology of these ST-segment changes is key because of the vastly different therapies used to treat them. We describe the case of a patient with massive transient J-waves and ST-segment elevation in the context of an intracranial hemorrhage.

Effect of ECG filter settings on J-waves.

BACKGROUND: While J-waves were observed in healthy populations, variations in their reported incidence may be partly explicable by the ECG filter setting. METHODS: We obtained resting 12-lead ECG recordings in 665 consecutive patients and enrolled 112 (56 men, 56 women, mean age 59.3±16.1years) who manifested J-waves on ECGs acquired with a 150-Hz low-pass filter. We then studied the J-waves on individual ECGs to look for morphological changes when 25-, 35-, 75-, 100-, and 150Hz filters were used. RESULTS: The notching observed with the 150-Hz filter changed to slurring (42%) or was eliminated (28%) with the 25-Hz filter. Similarly, the slurring seen with the 150-Hz filter was eliminated on 71% of ECGs recorded with the 25-Hz filter. The amplitude of J-waves was significantly lower with 25- and 35-Hz than 75-, 100-, and 150-Hz filters (p<0.0001). CONCLUSIONS: The ECG filter setting significantly affects the J-wave morphology.

ST-segment elevation myocardial infarction vs. hypothermia-induced electrocardiographic changes: a case report and brief review of the literature.

BACKGROUND: Diagnosed ST-segment elevation myocardial infarction (STEMI) usually prompts rapid cardiac catheterization response. OBJECTIVE: Our aim was to raise awareness that hypothermia can cause electrocardiographic (ECG) changes that mimic STEMI. CASE REPORT: Emergency Medical Services (EMS) was called for altered mental status and lethargy in a 47-year-old man with a medical history of paraplegia. His history included hepatitis C, hypertension, seizures, anxiety, and recent pneumonia treated with i.v. antibiotics. When brought in by EMS, the patient was responsive only to painful stimuli. His blood glucose was 89 mg/dL; blood pressure was 80/50 mm Hg, and ECG showed ST elevations diffusely. His vital signs in the emergency department were heart rate 53 beats/min, blood pressure 134/79 mm Hg, respiratory rate 14 breaths/min, pulse oximetry of 100%, and a rectal temperature of 32.7°C (91°F). A second ECG showed diffuse ST elevation, sinus bradycardia with a rate of 56 beats/min, and a first-degree atrioventricular block. J waves were noted in V3-V6, I and II. There were no reciprocal changes or ST depressions. A bedside ultrasound showed no pericardial effusion. The patient underwent cardiac catheterization, which showed no coronary artery disease and a normal ejection fraction. Later, hypercapneic respiratory failure with bilateral pneumonia developed and was intubated. His ECG the following day, once he was rewarmed, showed complete resolution of ST elevation and almost complete resolution of J waves. CONCLUSION: Obtaining a complete set of vital signs is key to making a correct diagnosis. Hypothermia should be considered in the differential diagnosis of ST elevation.

Detecting Subtle Osborn Waves in Hypothermia: A Case Report.

J waves, or Osborn waves, are a notable EKG finding in hypothermia, often appearing as prominent deflections but sometimes manifesting subtly. We report a 78-year-old female with moderate hypothermia (87.9°F) presenting with sinus bradycardia and subtle J waves on her EKG. After rewarming, these J waves resolved. Hypothermia management should prioritize gentle handling to avoid arrhythmias and ensure rapid rewarming during cardiopulmonary resuscitation. Continuous monitoring is crucial, as J waves can indicate a higher risk of ventricular fibrillation and cardiac arrest.

Triggers of Ventricular Fibrillation in Patients With Inferolateral J-Wave Syndrome.

BACKGROUND: There are few data on ventricular fibrillation (VF) initiation in patients with inferolateral J waves. OBJECTIVES: This multicenter study investigated the characteristics of triggers initiating spontaneous VF in inferolateral J-wave syndrome. METHODS: A total of 31 patients (age 37 ± 14 years, 24 male) with spontaneous VF episodes associated with inferolateral J waves were evaluated to determine the origin and characteristics of triggers. The J-wave pattern was recorded in inferior leads in 11 patients, lateral leads in 3, and inferolateral leads in 17. RESULTS: The VF triggers (n = 37) exhibited varying QRS durations (176 ± 21 milliseconds, range 119-219 milliseconds) and coupling intervals (339 ± 46 milliseconds, range 250-508 milliseconds) with a right (70%) or left (30%) bundle branch block (BBB) pattern. Trigger patterns were associated with J-wave location: left BBB triggers with inferior J waves and right BBB triggers with lateral J waves. Electrophysiologic study was performed for 22 VF triggers in 19 patients. They originated from the left or right Purkinje system in 6 and from the ventricular myocardium in 10 and were undetermined in 6. Purkinje vs myocardial triggers showed distinct electrocardiographic characteristics in coupling interval and QRS-complex duration and morphology. Abnormal epicardial substrate associated with fragmented electrograms was identified in 9 patients, with triggers originating from the same region in 7 patients. Catheter ablation resulted in VF suppression in 15 patients (79%). CONCLUSIONS: VF initiation in inferolateral J-wave syndrome is associated with significant individual heterogeneity in trigger characteristics. Myocardial triggers have electrocardiographic features distinct from Purkinje triggers, and their origin often colocalizes with an abnormal epicardial substrate.

The Stanford/PAVA data collection form for coding J waves on routine screening 10second ECGs.

The study of J waves and slurs and their association with cardiovascular death is clouded by the lack of a standardized coding or classification methodology. Over the past three years of studying these ECG patterns, we have evolved a Data Entry Form that is designed to resolve some of the key issues. These issues include the effect of other ECG findings, whether the QRS-ST junction occurs before or after the J waves, if contiguous leads are required and rules to distinguish J waves from fragmented QRS complexes. This form is now being used to code the ECGs of 44,000 VA patients and the follow up is being extended to 15years to resolve these issues.

Predictive effect of J waves on cardiac compression and clinical prognosis of esophageal tumors: a retrospective study.

Background: The J wave syndromes (JWS) could be observed in patients with mediastinal tumors, though few studies have verified the statistical correlation between J waves and cardiac compression by tumors. This study aimed to investigate the relationship between J waves and cardiac compression by esophageal tumor and to compare the prediction of J waves on clinical prognosis with that of cardiac compression by esophageal tumor. Methods: We enrolled 273 patients (228 males, 45 females; mean 63.8±7.5 years) with esophageal tumors admitted to Shanghai Chest Hospital between August 2016 and November 2020. The J wave was defined as a J-point elevation of ≥0.1 mV in a 12-lead electrocardiogram (ECG) and classified into multiple types. Chest computed tomography (CT) was reviewed to clarify the anatomical relationship between the heart and the esophageal tumor. The prognosis of severe cardiac events and survival status were followed up through medical history, examination records and telephone records. Results: J waves were present in 141 patients among all 273 cases. The sensitivity and specificity of cardiac compression by the tumor for J waves were 78.1% and 67.3%, respectively. The odds ratio (OR) of cardiac compression by the tumor to J waves was 7.33 [95% confidence interval (CI): 4.21-12.74; P<0.001]. The Kappa coefficient between J waves and cardiac compression was 0.44±0.05. The significance association between J waves and cardiac compression was independent from other clinical variables (P<0.001). Decreased J wave amplitude was correlated with the disappearance of cardiac compression during follow-up (P=0.03). Patients with J waves had a higher risk of severe cardiac events than those without J waves (OR =2.84, 95% CI: 1.22-6.63; P=0.01). During the follow-up period, we found that the presence of J waves [hazard ratio (HR) =2.28; 95% CI: 1.35-3.84; P=0.002] and cardiac compression by the tumor (HR =2.51; 95% CI: 1.51-4.17; P<0.001) were both negatively correlated with the survival time of patients. Conclusions: The presence of J waves could be used as an effective mean to predict the mechanical impact of esophageal tumor on the heart, and played an important role in predicting the survival of patients.

Contrast-induced early repolarization pattern and ventricular fibrillation.

Malignant arrhythmias during coronary angiography consist a complication of the procedure. Clinicians should be aware that intracoronary infusion of contrast medium can lead to physiological changes that lower the ventricular fibrillation threshold.

Dynamicity of hypothermia-induced J waves and the mechanism involved.

BACKGROUND: J waves develop during hypothermia, but the dynamicity of hypothermia-induced J waves is poorly understood. OBJECTIVE: The purpose of this study was to investigate the mechanism of the rate-dependent change in the amplitude of hypothermia-induced J waves. METHODS: Nineteen patients with severe hypothermia were included (mean age 70 ± 12 years; 16 men [84.2%]). The rectal temperature at the time of admission was 27.8° ± 2.5°C. In addition to prolonged PR, QRS complex, and corrected QT intervals, the distribution of prominent J waves was widespread in all 19 patients. RESULTS: Nine patients showed changes in RR intervals. When the RR interval shortened from 1353 ± 472 to 740 ± 391 ms (P = .0002), the J-wave amplitude increased from 0.50 ± 0.29 to 0.61 ±0.27 mV (P = .0075). The J-wave amplitude increased in 7 patients (77.8%) and decreased in 2 patients (22.2%) after short RR intervals. The augmentation of J waves at short RR intervals was associated with a significant prolongation of ventricular activation time (35 ± 5 ms vs 46 ± 5 ms; P = .0020), suggesting accentuated conduction delay. Increased conduction delay at short RR intervals was suggested to accentuate the phase 1 notch of the action potential and J waves in hypothermia. None developed ventricular fibrillation, and in 2 of 9 patients with atrial fibrillation, atrial fibrillation persisted after rewarming to normothermia. CONCLUSION: J waves in severe hypothermia were augmented after short RR intervals in 7 patients as expected for depolarization abnormality, whereas 2 patients showed a bradycardia-dependent augmentation as expected for transient outward current-mediated J waves. Increased conduction delay at short RR intervals can be responsible for the accentuation of the transient outward current and J waves during severe hypothermia.

The J-waves of hypothermia.

Prominent J-waves are observed in several clinical conditions many of which are highly arrhythmogenic and may lead to ventricular fibrillation (VF) and/or sudden cardiac death. We present the case of a 34-year-old male patient with hypothermia. Prominent J-waves (Osborn waves) and prolonged QT interval was evident in nearly every lead. Early recognition of these arrhythmogenic electrocardiogram (ECG) findings and treatment of hypothermia is important to minimize the risk of arrhythmic events.