A middle-aged male had 45 minutes of chest discomfort and drove to the ED. He has a history of hyperlipidemia. No previous MI.
His initial BP was 152/102, pulse 76.
Here is his triage ECG:
|Obvious anterolateral STEMI. Notice there are already well formed Q-waves. Q waves form in 1/2 of anterior MI within the first hour (Raitt et al.)
The cath lab was activated, aspirin and ticagrelor and a heparin bolus were given, and another ECG was recorded while waiting for the cath team to arrive in off hours:
|There are now multiform PVCs.
There are 4 PVCs in the 10 seconds recorded in lead II. But they are not all captured for every lead on the printed pdf 12-lead.
On the McKesson system, however, one can scroll through all 10 seconds of each lead. I have done so below in order to show the PVCs in all leads, including leads V1-V3:
|Now one can see easily that the PVCs (complexes 3 and 4 in leads V1-V3) are of a right bundle pattern. This means they originate in the LV. Notice that there is concordant ST elevation (STE in the same direction as the R’-wave). This makes the STEMI even more obvious.
Notice also that there is a very short coupling interval:
The first PVC occurs 320 ms after the initiation of the normal QRS, and it almost occurs directly on the T-wave.
So this is almost an R on T.
Here I magnify that area:
|The second beat here, which is the first PVC, is almost on the T-wave
The K was 3.4 mEq/L. Lactate 4.8 (this suggests some shock, but did not correlate with the rest of the clincical picture). K was given.
The interventionalist was concerned about the multiform PVCs with short coupling interval
The defibrillation pads were placed, and the interventionalist asked that metoprolol 5 mg IV be given prior to cath. It was given, and the PVCs stopped.
The first troponin I was less than 0.010 ng/mL (below the level of detection). (Remember this the next time someone tells you that it cannot be an MI because the troponin is negative; 50% of STEMI have an initial troponin less than the 99% URL, and many below the level of detection.)
An LAD occlusion proximal to a large 2nd diagonal was found and opened and stented.
The peak troponin was 75 ng/mL.
He received oral metoprolol after cath.
Contrast Echo done after cath:
Moderately reduced left ventricular systolic function. The estimated ejection fraction is 36%.
Regional wall motion abnormality-distal septum anterior and apex.
24 hours ECG:
|QS-waves (significant myocardial loss of septum and anterior wall)
There is still quite a bit of ST elevation and tall T-waves, suggesting some degree of “No-Reflow” (downstream plugging of small vessels with platelet-fibrin aggregates causing persistent ischemia)
At about 47 hours, he had a run of Ventricular Tachycardia. (Any VT beyond 48 hours in a patient without persistent or recurrent ischemia, there is consideration of an ICD. This patient barely met the cutoff)
However, no Reflow, with persistent ischemia, may explain the borderline late VT.
|Terminal T-wave inversion suggests some possible additional reperfusion.
|Not much change
PVCs and risk of VT
It may be that multiform PVCs, especially PVCs with a short coupling interval, put the patient at high risk of VT/VF, but as far as I can tell, it is not definitely proven in the literature (see a couple references below). PVCs of any coupling interval do increase the risk of VT/VF, as all VT/VF is initiated by a PVC. But it hasn’t been proven, as far as I can tell, that suppressing them increases or decreases risk.
In the CAST trial (cardiac arrhythmia suppression trial) of patients with previous, but not acute, MI and low ejection fraction and PVCs, patients whose PVCs were suppressed in a trial period of Type 1 antidysrhythmic (encainide, flecainide, or moricizine) were randomized to a type 1 vs. placebo. Results: those who received the anti-dysrhythmic had a higher risk of sudden arrhythmic death.
So type I antidysrhythmics are dangerous for this population (again, not the acute MI population).
PVCs and coupling intervals
This study suggests that short coupling intervals do increase the risk for Monomorphic ventricular tachycardias. VT can usually be witnessed to be initiated by PVCs.
This study which was much smaller, from 1974, contradicts that:
So what can we do to decrease the risk of VT/VF in this patient?
—class II antidysrhythmic in the Vaughan Williams classification)
–I won’t be discussing class I (e.g. lidocaine, Ib) or III (e.g. amiodarone) antidysrhythmics here.
Beta blockers decrease the incidence of ventricular fibrillation, and are overall beneficial for a stable subgroup of anterior STEMI who will undergo PCI (see details below), but for a less stable subgroup, they increase the risk of cardiogenic shock. Until 2005, early (ED) beta blockers were mandated for patients with acute MI. But all the data in their support had come from the pre-reperfusion era. Then the COMMIT trial of patients with STEMI receiving thrombolytics (2005, described in detail below) showed they lead to a decreased incidence of v fib, but increased incidence of cardiogenic shock, and overall no difference in mortality. Interestingly, the decrease in ventricular fibrillation by giving early beta blockers was a decrease in v fib after day 1. Later trials of subgroups with a lower risk of cardiogenic shock who are undergoing PCI showed modest probable benefit of early beta blockade without the adverse effects.
Bottom Line: If there are no contraindications (no heart failure, SBP at least 120, no tachycardia, no AV block), metoprolol 5mg IV x 3, with oral metoprolol given later if tolerated, seems to convey benefit prior to PCI in anterior MI.
Anterior MI patients treated with PCI (not fibrinolytics) without contraindications to beta blockers, who are anticipated to undergo PCI within 6 hours of onset, who have a BP greater than 120 systolic, appear to benefit from 3 5 mg doses of IV metoprolol given prior to PCI. All patients without contraindications benefit from oral metoprolol after PCI.
Our patient above fits this.
The best strategy may be to give esmolol bolus and drip which is a very short acting beta blocker that can be turned off at the first sign of cardiogenic shock.
Finally, there is little evidence that beta blockers are more important in patients with ventricular dysrhythmias, including frequent PVCs and short coupling intervals, but at least there is some face validity to this idea and randomized trials seem to show benefit without showing harm in this subgroup who are not at high risk of cardiogenic shock.
5 key references
1. Recommendations of the European Society of Cardiology 2017 guidelines for STEMI.
7.3.1 Early intravenous beta-blocker administration
Based on the current available evidence, early administration of i.v. beta-blockers at the time of presentation followed by oral beta-blockers should be considered in haemodynamically stable patients undergoing primary PCI.
In patients undergoing fibrinolysis, early i.v. beta-blocker treatment reduces the incidence of acute malignant ventricular arrhythmias, although there is no clear evidence of long-term clinical benefit.344–346
In patients undergoing primary PCI, the Effect of Early Metoprolol in Cardioprotection During an Acute Myocardial Infarction by Ibanez et al. (METOCARD-CNIC) trial (n = 270)
(and this long term followup
by Pizarro et al., see description below) showed that the very early administration of i.v. metoprolol (15 mg) at the time of diagnosis in patients with anterior STEMI, no signs of heart failure, and SBP at least 120 mmHg was associated with a reduction in infarct size measured by CMR at 5–7 days (25.6 g vs. 32.0 g; P
= 0.012), and higher LVEF at 6 months CMR (48.7% vs. 45.0%; P
= 0.018) compared with control treatment.347,348
All patients without contraindications received oral metoprolol within 24 h. The incidence of MACE (composite of death, admission as a result of heart failure, reinfarction, or malignant ventricular arrhythmias) at 2 years was 10.8% vs. 18.3% in the i.v. metoprolol and control arms (P
Metoprolol treatment was associated with a significant reduction in the incidence and extent of MVO.349 Roolvink et al. The Early Intravenous Beta-Blockers in Patients With ST-Segment Elevation Myocardial Infarction Before Primary Percutaneous Coronary Intervention (EARLY-BAMI) trial
randomized 683 patients with STEMI within 12 h of onset to i.v. metoprolol (5 mg at recruitment and an additional 5 mg immediately before PCI) or placebo.350
All patients without contraindications received oral metoprolol within 12 h. Early i.v. metoprolol administration did not show any benefit in reducing CMR-based infarct size, the trial primary endpoint, available only in 342 patients (55%), or the level of cardiac biomarker release. Early i.v. metoprolol was associated with a borderline reduction of malignant ventricular arrhythmias (3.6% vs. 6.9%; P = 0.050).
Patients treated with i.v. metoprolol showed no increased risk of haemodynamic instability, atrioventricular (AV) block, or MACE at 30 days. Post hoc
analyses from primary PCI trials testing other hypotheses have suggested that early i.v. beta-blocker administration might be associated with a clinical benefit, but a selection bias cannot be excluded even after correction for imbalances in baseline characteristics.351,352 Based on the current available evidence, early administration of i.v. beta-blockers at the time of presentation followed by oral beta-blockers should be considered in haemodynamically stable patients undergoing primary PCI.
7.3.2 Mid- and long-term beta-blocker treatment
Based on the current evidence, routine administration of beta-blockers in all post-STEMI patients should be considered as discussed in detail in the heart failure guidelines;6
beta-blockers are recommended in patients with reduced systolic LV function (LVEF ≤40%), in the absence of contraindications such as acute heart failure, haemodynamic instability, or higher degree AV block. Agents and doses of proven efficacy should be administered.357–361
As no study has properly addressed beta-blocker duration to date, no recommendation in this respect can be made. Regarding the timing of initiation of oral beta-blocker treatment in patients not receiving early i.v. beta-blockade, a retrospective registry analysis on 5259 patients suggested that early (i.e. 362