J waves may be observed during coronary angiography (CAG), but they have not been fully studied. We investigated the characteristics of J waves in 100 consecutive patients during CAG. The patients and their family members had no history of cardiac arrest. Approximately 60% of patients had ischemic heart disease, previous myocardial infarction, or angina pectoris, but at the time of this study, the right coronary artery was shown to be normal or patent after stenting. Electrocardiogram was serially recorded to monitor J waves and alteration of the QRS complex during CAG. In 12 patients (12%), J waves (0.249 ± 0.074 mV) newly appeared during right CAG, and in another 13 patients (13%), preexisting J waves increased from 0.155 ± 0.060 mV to 0.233 ± 0.133 mV during CAG. Left CAG induced no J waves or augmentation of J waves. Distinct alterations were observed in the QRS complex during CAG of both coronary arteries. Mechanistically, myocardial ischemia induced by contrast medium was considered to result in a local conduction delay, and when it occurred in the inferior wall, the site of the late activation of the ventricle, the conduction delay was manifested as J waves. In conclusion, J waves were confirmed to emerge or increase during angiography of the right but not the left coronary artery. Myocardial ischemia induced by contrast medium caused a local conduction delay that was manifested as J waves in the inferior wall, the site of the late activation of the ventricle.
J waves defined as notches or slurs of ≥0.1 mV in two or more contiguous leads at the terminal part of the QRS complex on a surface electrocardiogram (ECG) can be found in idiopathic ventricular fibrillation in the general population and other clinical situations and is categorized as the J-wave syndrome. , However, the mechanisms underlying J waves in each subset of J-wave syndrome have not been fully elucidated whereas some electrocardiographic characteristics have been noted: an augmentation of J-wave amplitude during bradycardia , or an augmentation of J-wave amplitude during tachycardia , that may be used in differentiating the mechanisms of J waves. We have previously reported cases with J waves developing during coronary angiography (CAG), and hereby, we investigated the occurrence or modulation of J waves during CAG.
ECGs were investigated for J waves during CAG in 100 patients who underwent CAG at our institution between August 2019 and March 2020. Patients were selected consecutively, but they were excluded if they had an acute myocardial infarction, unstable hemodynamics, ventricular tachyarrhythmia, and Wolff-Parkinson-White syndrome or bundle branch block. All patients with any individual or family history of cardiac arrest were denied. Clinical characteristics were obtained from the clinical chart. Heart failure was diagnosed from clinical history, the ejection fraction on echocardiography, or from the serum brain-type naturiuretic peptide level.
After written informed consent was obtained, cardiac catheterization was undertaken, and CAG was performed in a standardized manner using 4 to 6 ml of iopamidol in each injection. Serial ECGs were recorded before and throughout the administration of contrast medium continuing for several seconds after the end of the administration.
J waves were diagnosed when the J-wave amplitude was ≥0.1 mV and absent when the J-wave amplitude was <0.1 mV, and the prevalence of patients with J waves ≥0.1 mV was surveyed at the baseline. When J waves were ≥0.1 mV, the J-wave amplitude was measured at baseline and compared with the peak amplitude during CAG. The incidence of a new emergence of J waves ≥0.1 mV during CAG was also determined in patients with negative J waves (<0.1 mV) at baseline.
The effects of contrast medium on the activation pattern over the ventricle were evaluated from changes in the QRS morphology and changes in the R-wave amplitude in leads II and V 5 at baseline and during CAG. The maximum change in R-wave amplitude was compared in these leads and also between right and left CAG. Heart rate was determined from the ECGs.
Finally, patients were divided into 2 groups, one showing diagnostic J waves (≥0.1 mV) at baseline or during CAG and the other without J waves at baseline or during CAG, and the clinical and ECG characteristics were compared. When atrial premature contraction occurred, the J-wave amplitude was measured on the beat at a shorter RR interval to see the rate dependency of the J-wave amplitude. The changes in the R-wave amplitude in leads II and V 5 were compared between the 2 groups and between the right and left CAG.
Numerical data are presented as the mean ± SD, and categorical parameters are presented as the absolute number or percentage. Numerical data were compared by one-way ANOVA and analyzed by paired or unpaired t test. Categorical variables were compared by the chi-square test. A two-sided nominal p <0.05 was considered significant. Statistical analysis was performed using JMP Statistical Discovery Software (Version 5.0.1J. SAS Institute Inc., Cary, NC).
This retrospective case study was performed following the Declaration of Helsinki for Ethical Principles for Medical Research Involving Human Subjects and approved by the Institutional Review Board of Tachikawa Medical Center.
Results
The patients’ clinical characteristics are listed in Table 1 . The mean age was 68.3 ± 14.1 years, and 87% of participants were men. In the majority of cases, angiography was performed to evaluate previous percutaneous coronary intervention for acute myocardial infarction or angina pectoris. A total of 11 patients underwent CAG before transaortic valve replacement. Comorbidities were controlled by medication and no patient complained of chest pain or distress during CAG. Including the patients who had been treated by stenting, no significant stenosis lesions were present in the right coronary artery.
| Variable | All (n=100) | J waves No (n=75) | J waves Yes (n=25) | P-value |
|---|---|---|---|---|
| Men | 87 (87.0%) | 66 (88.0%) | 21 (84.0%) | 0.6135 |
| Age (years) | 68.3±14.1 | 67.7±14.9 | 70.0±11.8 | 0.4925 |
| Left ventricular ejection fraction (%) | 56±10 | 54±12 | 60±4 | 0.0874 |
| Serum creatinine (mg/dL) | 0.89±0.66 | 0.97±0.36 | 0.77±0.93 | 0.2481 |
| Estimated glomerular filtration rate (mL/min/1.73 m 2 ) | 62±20 | 59±19 | 72±20 | 0.0548 |
| Systolic blood pressure (mmHg) | 123±21 | 121±21 | 128±22 | 0.2128 |
| Diastolic blood pressure (mmHg) | 69±10 | 68±14 | 71±13 | 0.4952 |
| Comorbidities | 50 (50.0%) | 36 (48.0%) | 14 (56.0%) | 0.488 |
| Hypertension | 33 (33.0%) | 24 (32.0%) | 9 (36.0%) | 0.5553 |
| Diabetes mellitus | 51 (51.0%) | 38 (50.7%) | 13 (52.0%) | 0.908 |
| Dyslipidemia | 9 (9.0%) | 8 (10.7%) | 1 (4.0%) | 0.2759 |
| Hyperuricemia | 59 (59.0%) | 45 (60.0%) | 14 (56.0%) | 0.7253 |
| Ischemic heart diseases Valvular heart disease | 13 (13.0%) | 8 (10.7%) | 5 (20.0%) | 0.2481 |
| Cardiomyopathy | 4 (4.0%) | 3 (4.0%) | 1 (4.0%) | 1 |
| Congestive heart failure | 8 (8.0%) | 7 (9.3%) | 1 (4.0%) | 0.3625 |
| Chronic kidney disease | 3 (3.0%) | 2 (2.7%) | 1 (4.0%) | 0.7428 |
| Miscellaneous | 6 (6.0%) | 3 (4.0%) | 3 (12.0%) | 0.1731 |
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