[Improvement of postinfarct left myocardial contractile function after administration of diltiazem]
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Published on: December 11, 2017
G Gambelli1, R Donati, R Mezzanotte
1Divisione di Cardiologia, Ospedale G.B. Grassi, Roma.
Insights
Intravenous diltiazem, a calcium-channel blocker, effectively enhanced contractility in stunned myocardium post-myocardial infarction. This finding suggests potential therapeutic implications for selected patients.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Pharmacology
Background:
- Intracellular calcium imbalance is key in stunned/hibernating myocardium post-myocardial infarction.
- Recognizing these myocardial states impacts treatment and prognosis.
- Calcium-channel blockers show protective effects against myocardial reperfusion injury.
Purpose of the Study:
- To assess intravenous diltiazem's efficacy in improving contractility of viable, akinetic myocardium.
- To evaluate diltiazem, a calcium-channel blocker with negative inotropic effects, in post-myocardial infarction patients.
Main Methods:
- Sixty patients with acute myocardial infarction underwent dobutamine-echocardiography and diltiazem-echocardiography.
- Diltiazem was administered intravenously (0.25-1 mg/kg) with monitoring of left ventricular function (WMSI), ECG, and blood pressure.
- Results were compared to dobutamine tests, and a subset of 13 patients had post-revascularization echocardiograms.
Main Results:
- Diltiazem enhanced regional left ventricular contractility in 31 patients, compared to 28 with dobutamine.
- High correlation found between diltiazem and dobutamine WMSI (r=0.86) and post-procedure WMSI (r=0.91).
- Both tests showed high concordance in positive and negative responses.
Conclusions:
- Acute intravenous diltiazem administration can improve contractility in viable akinetic ventricular segments post-myocardial infarction.
- Findings suggest reconsidering calcium-channel blockers, like diltiazem, for selected post-myocardial infarction patients.
- The study has physiopathological and therapeutic implications for managing myocardial stunning and hibernation.
Background:
The impairment of intracellular calcium homeostasis is an important biochemical alteration in stunned and hibernating myocardium. These different forms of viable myocardium frequently occur after myocardial infarction and their recognition may modify the therapeutic program and prognosis. Experimental studies and experiences on male subjects have demonstrated that calcium-channel blockers exert a protective action on myocardial reperfusion injury and reduce infarct size.
Objectives:
The aim of the present study was to evaluate the efficacy of i.v. diltiazem (i.e. a calcium-channel blocker with negative inotropic effect) in enhancing the contractility of viable akinetic myocardium in patients after myocardial infarction.
Methods:
Sixty patients (52 males and 8 females, age 57 +/- 10 years) with the first acute myocardial infarction were evaluated with dobutamine-echocardiography 9 +/- 2 days after admission and on the following day with diltiazem-echocardiography. Diltiazem was administered i.v. using repeated boluses of 0.25 mg/kg up to the maximum dose of 1 mg/kg. Before and during the infusion, left ventricular regional function was scored and the Wall Motion Score Index (WMSI) was calculated; ECG and arterial blood pressure were also monitored. Results were compared with low-dose dobutamine-echocardiography. In a subset of 13 patients who underwent myocardial revascularization (7 coronary artery by-pass graftings and 6 percutaneous transluminal angioplasties), post-procedure echocardiograms were performed to evaluate whether regional left ventricular function had improved.
Results:
Low-dose dobutamine and diltiazem enhanced regional left ventricular contractility in 28 and 31 patients, respectively; both tests were positive in 26 cases. Conversely, dobutamine-test was negative in 32 patients and diltiazem in 29, with concordance in 27. A good correlation was found between diltiazem and dobutamine WMSI at the basal evaluation (r = 0.91; p < 0.000) as well as during the pharmacological test (r = 0.86; p < 0.000). In patients who underwent myocardial revascularization, the same good correlation was found between diltiazem-WMSI and WMSI evaluated after the procedure (r = 0.91; p < 0.000).
Conclusions:
Acute i.v. administration of diltiazem about ten days after myocardial infarction may enhance the contractility of viable akinetic ventricular wall segments, as evaluated with echocardiography. The results of this study may have some physiopathological and therapeutical implications that could lead to reconsidering the use of calcium-channel blockers, particularly diltiazem, in selected patients after myocardial infarction.
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