VIENNA, AUSTRIA — Perhaps another good reason to ensure optimal medical therapy (OMT) before implanting an implantable cardioverter defibrillator (ICD): the risk of heart-failure decompensation is increased in the months after an ICD shock but may be less likely if the patient is on optimal beta-blockade at the time of the shock,[1].
In a small series of patients with low LVEF driving their indication for an ICD who received an appropriate or inappropriate device shock, about one-fifth experienced HF decompensation over a mean follow-up of 3.4 years.
In this postshock cohort, the incidence of heart-failure decompensation fell by 59% (P<0.001) among those taking beta-blockers vs not taking beta-blockers. Cardiac mortality was reduced by about three-fourths in those on beta-blockers (P<0.001).
“We have observed that this effect is dose dependent: the higher the dose, the more benefit to the patient,” Dr Javier Jimenez-Candil (University Hospital of Salamanca, Spain) told theheart.org|Medscape Cardiology. The effect was especially significant and pronounced in the first 6 months following the shock.
Shocks from ICDs have been long seen in observational studies to increase mortality, independent of their reason for being—that is, terminating potentially fatal arrhythmias. The risk is observed whether the shocks are appropriate or inappropriate, with shock-induced myocardial structural damage along with sympathetic activation proposed as possible causes.
The current study, Jimenez-Candil said, supports the view that ICD shocks do induce sympathetic activation, a kind of “flight-or-fight” response that beta-blockers are exceptionally good at inhibiting, as a major cause of the resulting cardiovascular damage.
They also underscore the importance of OMT prior to deciding on an ICD for patient; in contrast to common practice in the US, Jimenez-Candil said, in Spain, clinicians are diligent about getting patients on OMT before they are considered for an implanted device.
Jimenez-Candil presented the analysis here at the European Heart Rhythm Association (EHRA) EUROPACE-CARDIOSTIM 2017 sessions.
He and his colleagues looked at 435 patients with LV dysfunction (mean LVEF 30%) and ICDs, about half in NYHA class 2 and the rest in class 3, 64% with ischemic cardiomyopathy, 62% getting the devices for primary prevention, and 61% on beta-blockers.
Of the 162 patients experiencing at least one shock over a mean follow-up of 3.4 years, shocks were appropriate in 91 patients, inappropriate in 44, and both appropriate and inappropriate in 27 patients.
Heart-failure decompensation ensued in 35.8% of the 162 patients experiencing any kind of shock vs 18.3% (P=0.006) of patients who remained shock-free. It occurred in 25.8% of patients on beta-blockers and 64.3% of those not on beta-blockers (P<0.001); the corresponding rates of cardiac death were 16% and 62% (P<0.001).
Post-Shock Incidence of Heart Failure Decompensation by Time from a First Shock
| Time of HF decompensation from first shock (mo) | Incidence on beta-blockers (%) | Incidence without beta-blockers (%) |
|---|---|---|
| 6 | 6 | 32a |
| 7–12 | 4 | 16b |
| 13–18 | 10 | 8 |
| 19–24 | 4 | 10 |
| 25–36 | 6 | 4 |
| 37–42 | 2 | 2 |
a. P<0.001 vs incidence on beta-blockers
b. P=0.03 vs incidence on beta-blockers
Four independent predictors of increased or decreased risk of postshock HF decompensation emerged in multivariate analysis:
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NYHA class: HR 2.2 (P=0.003).
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Serum creatinine: HR 2.4 (P=0.036).
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Number of shocks: HR 1.07 (P=0.008).
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Beta-blocker therapy: HR 0.35 (P<0.001).
The findings support shock-induced spikes in sympathetic activation as a major cause of postshock adverse cardiac events, according to Jimenez-Candil, and combined with other research, downplay such a role for shock-induced myocyte structural damage.
For example, he said, there’s evidence that shocks to the heart do not have any such sequelae if at the time the patient is under deep sedation, such as during a DC cardioversion for atrial fibrillation.
Jimenez-Candil said he has no relevant financial relationships.
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