What does this research mean for the field?

Inhibition of endogenous nitric oxide synthase with L-NMMA during adenylyl cyclase stimulation further increases left ventricular contractility (Emax) by 26% and reduces pressure-volume area by 9% without altering mechanical efficiency in patients with idiopathic dilated cardiomyopathy. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

January 1, 2007Circulation JournalOpen Access

Inhibition of Endogenous Nitric Oxide Synthase Augments Contractile Response to Adenylyl Cyclase Stimulation Without Altering Mechanical Efficiency in Patients With Idiopathic Dilated Cardiomyopathy

Q: What is the clinical evidence from this study?

Population: Heart failure due to idiopathic cardiomyopathy (n=13). Intervention: NG-monomethyl-L-arginine (L-NMMA) with colforsin daropate vs. Colforsin daropate alone. Primary outcome: Left ventricular hemodynamics and mechanoenergetics (Emax, EW, PVA, MVO2, mechanical efficiency).

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Key result

Inhibition of endogenous nitric oxide synthase with L-NMMA during adenylyl cyclase stimulation further increased Emax by 26% and reduced PVA by 9% without altering mechanical efficiency.

Why the study?

Does cardiac NOS inhibition with L-NMMA augment the contractile response to adenylyl cyclase stimulation with colforsin daropate in patients with idiopathic dilated cardiomyopathy?

Population

13 patients with heart failure due to idiopathic dilated cardiomyopathy, normal sinus rhythm, NYHA…

Comparison

Concurrent infusion of colforsin daropate and… vs Baseline and colforsin daropate infusion alone.

Design

Case_series

Follow-up

Acute (during cardiac catheterization)

Authors

SOSoichiro OhtaShinko Hospital TSToshiro ShinkeInterventional Cardiology KHKatsuya HataUniversity of Tsukuba

Discussion

Member takes

Implication

May augment adenylyl cyclase inotropic response in dilated cardiomyopathy without efficiency loss; hypothesis-generating, requires prospective trials before any clinical consideration.

Key Points

To determine how cardiac nitric oxide synthase inhibition influences left ventricular hemodynamics and mechanoenergetics during adenylyl cyclase stimulation in patients with heart failure.
Enrolled 13 patients with heart failure caused by idiopathic dilated cardiomyopathy.
Evaluated left ventricular contractility (Emax), external work, pressure-volume area, myocardial oxygen consumption, and mechanical efficiency using conductance and coronary sinus thermodilution catheters.
Administered colforsin daropate alone, followed by co-infusion with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA; 200 micromol).
Colforsin daropate infusion increased left ventricular contractility (Emax) by 53% and external work by 18%, while reducing pressure-volume area by 14%, with no alterations in myocardial oxygen consumption or mechanical efficiency.
Co-administration of colforsin daropate and L-NMMA further increased Emax by 26% and reduced pressure-volume area by 9%, without altering myocardial oxygen consumption or mechanical efficiency.

Structured PICO

Does cardiac NOS inhibition with L-NMMA augment the contractile response to adenylyl cyclase stimulation with colforsin daropate in patients with idiopathic dilated cardiomyopathy?

Population

13 patients (10 men, 3 women, mean age 56±13 years) with heart failure due to idiopathic dilated cardiomyopathy (IDC), normal sinus rhythm, NYHA functional class II (n=8) or class III (n=5), and left ventricular ejection fraction (LVEF) <40%.

Intervention

Concurrent infusion of colforsin daropate (0.5 μg/kg/min IV) and the nitric oxide synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA; 20 μmol/min intracoronary for 10 min).

Comparator

Baseline (control) and colforsin daropate infusion alone (0.5 μg/kg/min IV for 30-45 min).

Outcome

Left ventricular (LV) hemodynamics and mechanoenergetics, specifically Emax (index of LV contractility), LV external work (EW), pressure-volume area (PVA), myocardial oxygen consumption (MVO2), and mechanical efficiency (EW/MVO2).surrogate

Inhibition of endogenous nitric oxide synthase with L-NMMA augments the positive inotropic response to adenylyl cyclase stimulation without worsening myocardial mechanical efficiency in patients with idiopathic dilated cardiomyopathy.

Limitations

Lack of a control group in which vehicle solution was infused in place of L-NMMA
Possibility that L-NMMA may directly affect the LV contractile response to colforsin daropate rather than through NOS inhibition
Potential errors related to the assumption of a linear end-systolic pressure-volume relation (ESPVR)

Cite This Study

Ohta et al. (2007) studied Heart failure due to idiopathic cardiomyopathy (n=13). NG-monomethyl-L-arginine (L-NMMA) with colforsin daropate vs. Colforsin daropate alone was evaluated on Left ventricular hemodynamics and mechanoenergetics (Emax, EW, PVA, MVO2, mechanical efficiency). Inhibition of endogenous nitric oxide synthase with L-NMMA during adenylyl cyclase stimulation further increased Emax by 26% and reduced PVA by 9% without altering mechanical efficiency.

synapsesocial.com/papers/6a14f5f69ff8b2b0e129e019 https://doi.org/10.1253/circj.71.1268

Topics

Heart failure HFrEF treatment

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Implication

May augment adenylyl cyclase inotropic response in dilated cardiomyopathy without efficiency loss; hypothesis-generating, requires prospective trials before any clinical consideration.

Inhibition of Endogenous Nitric Oxide Synthase Augments Contractile Response to Adenylyl Cyclase Stimulation Without Altering Mechanical Efficiency in Patients With Idiopathic Dilated Cardiomyopathy

Discussion

Member takes

Implication

Key Points

Structured PICO

Limitations

Cite This Study

Topics

Inhibition of Endogenous Nitric Oxide Synthase Augments Contractile Response to Adenylyl Cyclase Stimulation Without Altering Mechanical Efficiency in Patients With Idiopathic Dilated Cardiomyopathy

Discussion

Member takes

Implication

Key Points

Structured PICO

Limitations

Cite This Study

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