Recovery Phase Of Exercise Test Research Articles

ST Elevation During Recovery Phase of Exercise Test

ST Elevation During Recovery Phase of Exercise Test

Listening to Heart Rate for Myocardial Ischemic Site

We describe a 63-year-old woman with severe stenosis in the right coronary artery. During the recovery phase of exercise testing, the monitor sound of heart rate changed rhythmically in a delicate fashion. Heart rate variability analysis revealed the association of the rhythm fluctuation with transient vagal enhancement. This phenomenon is known as Bezold-Jarisch reflex, which has been explained by the preferential distribution of cardiac receptors along afferent vagal pathways in the inferior wall of the left ventricle. After coronary angioplasty, the examiner could not notice the fluctuation of heart rate during the recovery phase of a restudy of exercise testing. Listening to heart rate fluctuation during exercise testing, although it may be rare, possibly helps examiners to estimate the site of ischemia to be in the inferior myocardium. doi:10.4021/jmc241e

Brugada syndrome: A brand new case

Brugada syndrome (BS) is a disorder characterized by syncope or sudden death associated with one of several electrocardiographic (ECG) patterns characterized by incomplete right bundle branch block and ST elevation in the anterior precordial leads. Patients with BS are prone to develop ventricular tachyarrhythmias that may lead to syncope, cardiac arrest, or sudden cardiac death. A 58-year-old woman is the first described case of Brugada syndrome in Serbia with intermittent typical changes in basic electrocardiography (ECG): ST segment elevation in the precordial chest leads like dome or coved--major form or type I. For the last 27 years the patient had suffered of palpitations and dizziness, without syncopal events. Her sister had died suddenly during the night in sleep. During 24-hour Holter monitoring the patient had ventricular premature beats during the night with R/T phenomenon and during the recovery phase of exercise testing had rare premature ventricular beats as the consequence of parasympatethic stimulation. Late potentials were positive. Echocardiography revealed left ventricular ejection fraction of 60%. We performed coronary angiography and epicardial coronary arteries were without significant stenosis and structural heart disease was excluded. In the bigining of the electrophysiological study ECG was normal, and after administration of Propaphenon i.v. Brugada syndrome unmasked with appearance of type I ECG pattern. A programed ventricular stimulation induced non sustained ventricular tachycardia. One-chamber implantable cardioverter defibrillator was implanted and the patient was treated with a combination od amiodarone and metoprolol per os. After one-year folow-up, there were no episodes of ventricular tachycardia and ventricular fibrillation. Brugada syndrome is a myocardial disorder which prognosis and therapy are related to presence of ventricular fibrillation or ventricular tachycardia. Electrophysiologicaly induced malignant ventricular disorders class I are indication for implantation of cardioverter defibrilator, as also occurred in presented patient.

Type I Brugada electrocardiogram pattern during the recovery phase of exercise testing

A 33-year-old Algerian man presenting with acute asthma was found to have right bundle branch block and anterior ST-segment elevation on surface electrocardiogram (ECG). Two years earlier he had suffered a syncopal event during which relatives were unable to find a pulse. A brother had died suddenly with acute asthma. Exercise tolerance …

The Relationship Between Heart Rate Recovery and Heart Rate Variability in Coronary Artery Disease

Reduced heart rate recovery (HRR) in coronary artery disease (CAD) is predictive of increased cardiovascular mortality and is related to reduced parasympathetic tonus. To investigate HRR and heart rate variability (HRV) measured at steady state condition and the relationship between these two parameters in CAD. In our study, we enrolled 33 (28 males, mean age 52.4 +/- 9.6 years) patients with CAD who did not have heart failure, atrial fibrillation, pacemaker, and any disease state that could affect the autonomic functions and 38 age-matched healthy subjects (21 males, mean age 48.3 +/- 7.8 years). All the patients underwent submaximal treadmill exercise testing (Bruce protocol). HRR was calculated by subtracting the heart rate values at the 1st, 2nd, and 3rd minutes of the recovery phase from the peak heart rate (HRR(1), HRR(2), HRR(3)). Before exercise testing, short-term steady state HRV analyses of all subjects were obtained with the time- and frequency-domain methods and were correlated to HRR. For frequency-domain analysis, low-frequency HRV (LF, 0.004-0.15 Hz), high-frequency HRV (HF, 0.15-0.5 Hz), and LF/HF ratio were measured for 5 minutes in the morning. For time-domain analysis, standard deviation of the normal-to-normal NN intervals (SDNN), square root of the mean squared differences of successive N-N intervals (RMSSD), and proportion derived by dividing the number of interval differences of successive N-N intervals greater than 50 ms by the total number of N-N intervals (pNN50) were obtained. Only HRR(3) was used for the correlation analysis. In CAD groups, the HF, an indicator of parasympathetic activation, was significantly reduced, whereas the LF and LF/HF values, which are indicators of sympathetic activity, were increased (P = 0.0001 for each parameter). The time-domain parameters SDNN, RMSSD, and pNN50 were significantly reduced in the patient group (P = 0.0001, P = 0.009, and P = 0.0001, respectively). Similar to the HRV parameters, the HRR(1), HRR(2), and HRR(3) values were significantly reduced in the patient group (P = 0.0001 for each parameter). We observed a significant negative correlation between HRR(3) and LF (r =-0.67, P = 0.0001) and between HRR(3) and LF/HF (r =-0.62, P < 0.0001), while there was a significant positive correlation between HRR(3) and HF, SDNN, RMSSD, and pNN50 (r = 0.69, P = 0.0001; r = 0.41, P = 0.0001; r = 0.31, P = 0.008; and r = 0.44, P = 0.0001). HRR and HRV are significantly reduced in CAD. The reduction in HRR is parallel to the changes in HRV parameters. HRR, which can be measured easily in the recovery phase of exercise testing, can be used to detect the depression of parasympathetic tonus and to evaluate the basal autonomic balance in this patient group.

Overall diagnostic performance of ST-segment depression at recovery phase of exercise test in detection of coronary artery disease

Overall diagnostic performance of ST-segment depression at recovery phase of exercise test in detection of coronary artery disease

Single coronary artery complicating repair of pulmonic stenosis

supplied an appreciable amount of anterior and inferior left ventricular myocardium. Dunn et al.’ found that exercise-induced ST segment elevation in ECG leads V, or aVL was highly specific for the presence of LAD coronary artery stenosis and reversible anterior wall myocardial ischemia. Alternatively, we cannot exclude the possibility that coexistent coronary vasospasm superimposed on a critical coronary stenosis was responsible for the observed exercise-induced ST segment elevation, although there were no associated clinical features or abnormal ST segment shifts during ambulatory ECG monitoring to support this. Weiner et al6 have previously described exercise-induced ST segment elevation during the recovery phase of exercise testing in four patients with variant angina, two of whom had associated fixed coronary stenoses. Three of their patients exhibited ST segment depression during exercise, and ST segment elevation was not observed until 2 or 3 minutes after the cessation of exercise.6 We hypothesize that this patient developed subendocardial &hernia manifested by ST segment depression at a significant level of exercise (rate-pressure product 25,000), which rapidly progressed to “silent” transmural myocardial ischemia at maximal exercise and early into recovery. Undoubtedly, the exercise test was continued beyond the point of diagnostic ischemic ST segment changes because of the patient’s asymptomatic status. The subsequent appearance of marked anterior wall ST segment elevation delineated the presence of a strikingly positive exercise study, which ultimately led to catheterization and angioplasty. We conclude that asymptomatic exercise-induced ST segment elevation in the absence of prior ECG Q waves may be a manifestation of significant “silent myocardial ischemia,” presumably due to highgrade fixed coronary artery disease and/or superimposed coronary vasospasm. These findings should prompt consideration for urgent invasive evaluation.