Is Local Nitric Oxide Availability Responsible for Myocardial Salvage after Remote Preconditioning?

Arroyo-Martínez, Esbeidira Aranet; Meaney, Alejandra; Gutiérrez-Salmeán, Gabriela; Rivera-Capello, Juan Miguel; González-Coronado, Vidal; Alcocer-Chauvet, Alejandro; Castillo, Genaro; Nájera, Nayelli; Ceballos, Guillermo; Meaney, Eduardo

doi:10.5935/abc.20160100

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Original Article • Arq. Bras. Cardiol. 107 (2) • Aug 2016 • https://doi.org/10.5935/abc.20160100 linkcopy

Is Local Nitric Oxide Availability Responsible for Myocardial Salvage after Remote Preconditioning?

Authorship SCIMAGO INSTITUTIONS RANKINGS

Abstract

Background: Remote ischemic preconditioning (RIPC) represents an attractive therapy for myocardial protection, particularly when ischemic events can be anticipated. Although several hypothetic mechanisms have been proposed, no definite molecular pathways have been elucidated.

Objective: We evaluated the effect of brachial circulation cuff occlusion on myocardial ischemic tolerance, necrosis, and nitric oxide (NO) in patients with ischemic heart disease undergoing elective percutaneous coronary interventions (PCI).

Methods: 46 patients were randomly allocated into two groups: control and RIPC before PCI procedures. Electrocardiographic analysis, serum concentrations of troponin I (cTn-I) were measured at baseline and 24 hours after PCI. A blood sample from the atherosclerotic plaque was drawn to determine nitrate and nitrites.

Results: RIPC increased the availability of NO in the stented coronary artery. Control patients presented a small but significant increase in cTn-I, whilst it remained unchanged in preconditioned group. The preconditioning maneuver not only preserved but also enhanced the sum of R waves.

Conclusions: RIPC induced an intracoronary increase of NO levels associated with a decrease in myocardial damage (measured as no increase in cTn-I) with electrocardiographic increases in the sum of R waves, suggesting an improved myocardium after elective PCI.

Keywords:
Nitric Oxide; Ischemia; Ischemic Preconditioning, Myocardial; Reperfusion

Variable	ControlGroup (n=23)		PreconditioningGroup (n=23)
Variable	x	SD	x	SD
Age (years)	66.1	11.3	63	6.9
Body mass index (kg/m²)	26.8	4.2	27.7	4.5
	n	%	n	%
Male	15	65	16	69
Type 2 diabetes mellitus	16	79	14	60.8
High blood pressure	19	83	21	91.3
Pharmacological treatment
Aspirin	23	100	23	100
Clopidogrel	23	100	23	100
β-blockers	13	57	18	78
ACEI	8	35	13	56
ARBs	11	48	7	30.4
CCB	5	21.7	6	26
Statins	19	82.6	21	91.3
Insulin	5	22	4	17.3
Metformin	16	70	11	47.8
Previous myocardial infarction	11	48	12	52
ST elevation (0.5-1 mV)	0	0	0	0
Baseline troponin I <0.04 ng/mL	23	100	23	100
Glomerular filtration rate (mL/min/1.73 m²)
< 15 (renal failure, stage V)	3	13	0	0
15-29 (severe reduction of GFR, stage IV)	4	17.3	3	13
30-59 (moderate reduction of GFR, stage III)	3	13	4	17.3
60-89 (mild reduction of GFR, stage II)	7	30.4	10	43
≥ 90 (normal GFR, stage I)	6	26	6	26

Total R summation (Σ)
Control Group, X±SD, mm			Preconditioning group, X±SD, mm
Σbasal	post PCI	p value	Σbasal	post PCI	p value
56.9±139	51.3±12.7	< 0.0001	53.3±230	62.0±22.4	0.006
Precordial R wave summation
Σbasal	Σpost PCI	p value	Σbasal	Σpost PCI	p value
36.5±21.8	32±17.9	0.003	33.1±18	37.3±19.5	0.057

Control			Preconditioning
Cr basal	Cr post PCI	p	Cr basal	Cr post PCI	p
mg/dL	mg/dL	value	mg/dL	mg/dL	value
1.28±0.63	1.39±0.67	0.001	1.0±0.32	1.17±0.36	0.002
GFR mL/min/1.73 m²			GFR mL/min/1.73 m²
Basal	Post-PCI		Basal	Post-PCI
63±26.5	57±23.5	0.003	72.0±21.1	64.4±20.97	<0.0001

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[TFN1] SD: standard deviation; GFR: glomerular filtration rate; ACEI: angiotensin-converting-enzyme inhibitors; ARBs: angiotensin II receptor blockers; CCB: calcium-channels blockers.