View Full Version : Significant increase in PVC's
04-22-2008, 02:18 AM
Well... I just spent most of the day at the ER and they found nothing.
For this past week, I have had a siginficant increase in PVC's. Usually, I might normally have a few PVC's in a week- lately I have been having 15-20 per day or more. Today, after ensuring I was well rested, I went to work and around lunch time was starting to have some PVC's- no other symptoms. I called my cardio at Mayo- the nurse advised me to go to the ER and get checked out. From 12:00pm to 5:00pm I counted 15 PVC's, from 5:00pm to 10:pm, I have counted about 10. At the hospital, I got a EKG (All normal), I had the best echo Ive ever had (all normal, resting avg gradient 20, valsalva 40), and my elctrolytes were normal. Magnesium was normal.
So whats up? Why am I getting these with this high frequency? The only change I have had recently is I have begun to excersize- I have been doing some biking on a trainer for 30 to 40 minutes; although I have missed the last 4 days.
I am sure this has happened to others before- can anyone shed any light?
04-22-2008, 01:16 PM
BOTTOM LINE: PVC's occur for various reasons... most concern and much uncertainty surrounds what PVC"S can mean for those w/ structural heart disease as HCM.
YOU SHOULD be checked by a specialist in HCM. I have a cazillion( my EP's words) PVC's each time my device is interrogated. I have an AICD. DO YOU?
04-22-2008, 01:20 PM
Prevalence and Prognostic Value of Exercise Arrhythmias
from American Heart Journal
EIVAs are common during exercise testing, and although researched extensively, their clinical significance remains poorly defined. Previous studies consistently suggest that the prevalence of EIVAs increases in older populations[2,5,6] and in those with cardiovascular disease.[2,4,21] Some studies suggest that EIVAs may result from exercise-induced ischemia, because the prevalence of EIVAs increases in those with ischemia[5,22]; however, other studies refute these results.[6,8,10,23,24]
The prognostic significance of EIVAs has also generated controversy. Some studies have shown that EIVAs are not strong predictors of mortality after recovery from myocardial infarction[8,24] and in patients with coronary artery disease (CAD). In a small study by Nair et al, frequent or complex exercise-induced PVCs did not predict 4-year mortality in patients with CAD. Sami et al and Weiner et al also reported that patients who experienced at least 1 PVC during exercise were not at increased risk of mortality during a 5-year follow-up period. More recently, Schweikert et al found that in patients with CAD with no history of severe ventricular ectopy at rest, exercise-induced frequent or complex PVCs were not predictive of 2-year mortality. Other studies of patients with known or suspected heart disease demonstrate that PVCs during exercise are associated with increased mortality.[3-5] In asymptomatic individuals, studies of those without known heart disease found no association between EIVAs and mortality[10,11]; however, Jouven et al recently reported that asymptomatic males with frequent exercise-induced PVCs had a 2.5-times greater risk of long-term mortality than males without EIVAs.
Inconsistency in study design is largely responsible for the discrepancies in these previous studies. Many earlier studies used small sample sizes and short follow-up periods. Sex of the study population most likely also affected the results. The Framingham study reported that while asymptomatic males with frequent or complex PVCs on ambulatory ECG were at increased risk of mortality, asymptomatic females were not. This study and findings by Jouven et al found EIVAs to be predictive of mortality when male populations were considered. Previous studies have used varying criteria to define EIVAs, with some studies considering EIVAs to be present if any PVC was recorded during exercise. The prevalence of EIVAs will be more reproducible on future exercise tests if frequent or complex PVCs are used as markers for EIVAs instead of occasional PVCs. In addition, others have documented an increased risk of mortality in those with frequent or complex PVCs during exercise compared with those with only occasional PVCs.[3,9] Finally, there is inconsistency in previous reports regarding the inclusion or exclusion of those with resting PVCs.
This study tried to address these limitations. A large sample size was used with a relatively long follow-up. The prognostic significance of EIVAs was compared between those with and without cardiovascular disease by use of the same methodology. Unlike many previous studies, ours took into consideration the presence of exercise-induced ischemia and resting PVCs when determining the prognostic utility of EIVAs.
We confirmed that the prevalence of EIVAs increased in those who have cardiovascular and/or pulmonary disease. By use of the log rank statistic, EIVAs were found to be predictive of mortality in those with and without disease. Although EIVAs were not a marker of mortality in those without disease after adjusting for age, in a univariate analysis, we found that the risk associated with EIVAs was nonsignificant early in follow up but became significant near the end of follow up. In the study by Jouven et al, EIVAs were long-term predictors of mortality in a healthy population. From these findings we hypothesize that the arrhythmic substrate responsible for EIVAs may pose no immediate risk for mortality, but individuals could become more susceptible to its effects with age. Aging is associated with loss of vagal tone and other processes that can result in myocardial fibrosis and ischemia, potentially lowering the threshold to arrhythmias later in life in those who are initially free of cardiovascular disease.
We found that ischemia (ST depression and/or angina) was associated with EIVAs because ischemia was more prevalent in the "EIVAs only" subgroup compared with those with resting PVCs with or without EIVAs and those with neither rest nor exercise ventricular ectopy. The presence of EIVAs added greater predictive power to the finding of exercise-induced ischemia alone.
Our findings indicate that resting PVCs were associated with the development of EIVAs. Although resting PVCs are associated with EIVAs, they do not seem to contribute additional prognostic information to the finding of resting PVCs alone. Further studies investigating EIVAs should differentiate those with resting PVCs from those without resting PVCs because this marker of the arrhythmic substrate impacts on the prevalence and prognostic significance of EIVAs.
Our findings are limited in that they are applicable only to men, which could be important due to possible sex differences in the prognostic significance of PVCs. In addition, we only had all-cause mortality data; we did not have specific cause of death nor were we able to censor on cardiovascular interventions. In the study by Jouven et al, EIVAs predicted mortality when both all-cause mortality and cardiovascular mortality were used as end points. Our "apparently healthy" group had no history of cardiovascular or pulmonary disease and had a normal exercise test response, but all of the patients in this group were referred for exercise testing within the Veterans Affairs health care system. However, echocardiograms might have detected cardiac disease in a portion of them either initially or during follow up.
Further limitations relate to our a priori determined coding of PVCs. Although this is a strength for hypothesis testing, we were unable to go back and recode our data. In fact, this strengthens our findings and supports further work in this area by now most assuredly considering resting PVCs. Our data were coded in terms of whether EIVAs were occasional or frequent in nature, but we did not precisely quantify the PVC rate at rest or during exercise, and therefore we could not determine the rate of increase with exercise. We did not code exercise PVCs as appearing solely during recovery and we did not code PVC morphology. Further investigations should examine how the morphology of EIVAs affects prognosis and, for those with PVCs at rest, whether the rate of increase of PVCs with exercise further influences mortality.
Finally, the increase in mortality associated with PVCs that we found was modest (slightly >1% annually) and there is no established therapy, making our findings of limited clinical significance.
Because EIVAs are associated with an increased risk for death, health professionals should encourage men with EIVAs, particularly those with known cardiopulmonary disease, to receive regular health maintenance, comply with established therapies, and to aggressively modify risk factors. Patients without cardiopulmonary disease should be reassured that EIVAs present no immediate risk but be reevaluated after 5 years.
04-22-2008, 01:22 PM
Recovery PVCs on exercise test are prognostic
February 1, 2008 Lisa Nainggolan
Palo Alto, CA - A new study shows that individuals undergoing treadmill testing who had ventricular arrhythmias during the recovery phase had an almost doubling of mortality in the five-year follow-up period, compared with those who had arrhythmias only during exercise . Dr Frederick E Dewey (Stanford University Medical School, Palo Alto, CA) and colleagues report their findings in the January 28, 2008 issue of the Archives of Internal Medicine.
Dewey told heartwire: "Recovery premature ventricular complexes [PVCs] seem to be more significant than PVCs that occur during exercise testing. They seem to have some prognostic significance, so that there appears to be additional risk stratification provided by arrhythmias during recovery," he noted. In contrast, PVCs occurring solely during exercise have limited prognostic significance, he said.
"Given the fact that there was a strong association with markers for ischemia with recovery PVCs, these patients might benefit from a more sensitive imaging modality for demonstrating (or not demonstrating) myocardial ischemia, such as myocardial perfusion imaging or exercise echo," he suggests.
Significance of exercise and recovery PVCs unclear
Dewey and colleagues explain that the relative prognostic significance of exercise and recovery-period ectopy has been unclear. "While some have found that recovery ectopy is more robustly associated with adverse prognosis than exercise ectopy, other results suggest otherwise." These apparent disparities may result from inconsistent methods, varied definitions of significant arrhythmia, differences in sample size and length of follow-up, or etiologic differences in PVCs in the various subject populations that have been studied, they note.
"We aimed in this study to evaluate the clinical correlates and relative prognostic significance of exercise and recovery PVCs in subjects referred for clinical exercise treadmill testing." They studied 1847 heart-failure-free patients who underwent exercise testing between March 1997 and January 2004 in the Veterans Affairs Palo Alto Healthcare System. About 55% of subjects had PVCs at some stage during exercise," Dewey noted; 46% developed exercise PVCs and 33.6% had recovery PVCs.
During 5.4 years of follow-up, 161 subjects (8.7%) died, and 53 of these deaths (32.9%) were due to cardiovascular causes. Recovery PVCs, but not exercise PVCs, were associated with 71% to 96% greater propensity-adjusted mortality rates (hazard ratio 1.96 for infrequent PVCs and HR 1.71 for frequent PVCs, compared with subjects without PVCs).
PVCs during exercise were associated with increased mortality rates only if accompanied by PVCs after exercise. But "similar to previous findings in clinical cohorts . . . recovery PVCs were robustly associated with adverse prognosis regardless of the presence of PVCs during exercise.
"Of note, the hazards for infrequent and frequent PVCs after exercise were similar, suggesting that the absolute presence of recovery PVCs has more prognostic significance than does the recovery PVC frequency," they add.
Occurrence of recovery PVCs reclassified 33.2% of subjects with intermediate-risk Duke Treadmill Scores into higher-risk subgroups.
Will statins reduce recovery PVCs?
Dewey et al go on to speculate on the possible mechanistic basis for their observations. Previous studies have suggested that age-associated fibrosis of the myocardium, ischemia, ventricular hypertrophy, and loss of vagal tone may lower the arrhythmic threshold, they note.
"A predisposition to or findings consistent with ischemia were associated only with recovery PVCs after adjustment for other variables in our population. Our findings suggest that this association was independent of other factors only in the recovery period," they note.
In contrast, both infrequent and frequent exercise PVCs were directly related to the heart-rate increase with exercise, likely resulting from increased sympathetic activity in subjects who were able to attain higher peak heart rates, they note.
Dewey told heartwire that the next step for his team is to look at interventions to see what might reduce the risk of arrhythmias during the recovery phase of exercise testing. Although many of the patients in this study were already taking statins, "a significant proportion were not," he noted, so they now plan to look at how statin use might reduce the rate of recovery PVCs.
Dewey FE, Kapoor JR, Williams RS, et al. Ventricular arrhythmias during clinical testing and prognosis. Arch Intern Med 2008; 168:225-234.
04-22-2008, 01:49 PM
YOU SHOULD be checked by a specialist in HCM. I have a cazillion( my EP's words) PVC's each time my device is interrogated. I have an AICD. DO YOU?
Those cazillion PVC's that you have- do you feel them a lot or do they happen for the most part without you feeling them? I do not have an AICD yet. I talked with Dr. Tajik three weeks ago in my last follow up- he told me that I am not in the high risk category and I am not in the low risk category. He is waiting to see how I respond to Rx treatment and lowering risk factors before he decides to outfit me with an AICD- he basically wants to see where I the treatment takes me before deciding.
Thanks for the research articles Pam.
04-22-2008, 03:04 PM
Hi Tony, I responded to your e-mail, but for those here .. NO mostly I am not aware of them and there are sooooo many that she says cazillion.
I do tend to feel what I believe are PVC's when I am resting or recovering from activity of the day. This is also when I get most of my chest pain. I believe personally that it has a lot to do w/ ischemia from the microvascular component of my HCM.
You will see the ischemia reference as well as recovery PVC's mentioned in the literature I posted.
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