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Pharmacology toprevent spasm inconduits

Guo- Wei He

Clinical incidence ofspasm inarterial grafts

Existence and prevalence ofspasm ofarterialgrafts

Internal thoracic artery spasm:currentprevalence

e current incidence of coronary artery bypass gra (CABG) spasm has been estimated at 0.43%. e rst report of early postoperative gra spasm as a clinical entity was in the le internal thoracic artery (ITA; also known as the internal mammary artery) gra in 1987. Subsequently it was reported that spasm could be a localized phenomenon or a diuse process, referred to as a ‘string sign’. ese clinical reports promoted intense physiological and pharmacological studies on the biological characteristics of the ITA to understand the nature of spasm. In an early study, the author of this chapter demonstrated that the contractility of the distal section of the ITA is inversely correlated to its diameter; that is, the smaller the diameter, the greater the tendency for spasm to develop. is strongly suggests that the distal end of the ITA should not be harvested thereby helping to prevent gra spasm. In any event, it is almost never necessary to use the distal ITA particularly in the era of skeletonized ITA harvest and composite arterial graing. Indeed, many surgeons consider it important to leave the distal bifurcation of the ITA intact on the chest wall to facilitate sternal healing.

e exact prevalence of spasm of arterial gras, particularly when it is mild, is unknown, as it may be asymptomatic. However, when spasm is severe and does not respond to standard pharmacological management, it can be lethal.–  Areport conrmed that perioperative vasospasm in native coronary arteries or gras is about 0.43% (25/ 5762 patients) in all CABG surgery. It is possible, however, that the incidence of vasospasm could be underestimated because there may be some patients whose gra spasm is either asymptomatic or responsive to the early use of vasodilator agents and therefore not diagnosed as spasm.

Spasm ofother arterialgrafts

A large body of literature has demonstrated that the radial artery (RA),, and gastroepiploic artery are particularly prone to spasm. Indeed, the revival of the use of the RA during CABG was, at least in part, due to the successful use of antispastic medications.

Possible mechanisms ofspasm

Vascular spasm reects a complicated physiological status within blood vessels and while its precise mechanism is still unclear, it is understood to be an extreme form of vasoconstriction. In general, vasoconstriction may be evoked by a number of stimulants including mechanical and/ or nerve stimulation, as well as vasoconstrictor substances (spasmogens).,,

Spasmogens in arterial gras are well studied,, and include endothelium- derived contracting factors (e.g. endothelin 1), prostaglandins (e.g. thromboxane A (TXA) or its mimetic prostaglandin Fα), α- adrenoceptor agonists (e.g. norepinephrine, methoxamine, and phenylephrine), platelet- derived substances (e.g. 5- hydroxytryptamine), and the cellular membrane depolarizing agent potassium as well as mast cells and histamine.

It must be emphasized that the intact endothelium may prevent spasm of the vessel by spontaneous (basal) release of a number of endothelium- derived relaxing factors such as nitric oxide (NO).

Fig. 40.1 illustrates the possible mechanisms of contraction (or

spasm) in vessels.

Pharmacology ofthe vasodilator agents used forarterialgrafts

Prevention of spasm may be accomplished by following some important principles such as maximally protecting the vessel during harvesting by using the least traumatic surgical techniques as well as pharmacological methods.

e pharmacology of the vasodilator agents used to prevent gra spasm is complex. In this chapter, a brief outline is presented of the most common vasodilator agents used clinically.

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Vasoconstrictors

(spasmogens)

VOC

TXA

Agonists

]

[Ca

ROC

IP3

TXA

PLC

GPCR

ETα etc

Kca

RhoA

GTP

[Ca2+]i

Calmodulin

Contraction

Phospho-myosin light

MLCK

Myosin light chain

TPFP S1

chain

Relaxation

NO EDHFPGI

[Ca2+]i

Rho kinase

Calcium sensitization

MLCP

Smooth muscle

Endothelium

AII

Fig.40.1 Schema of molecular mechanisms of smooth muscle contraction that may lead to spasm and the role of intact endothelium in prevention of

spasm. Contraction:vascular smooth muscle contraction is the summation of myosin light chain kinase (MLCK) and myosin light chain phosphatase (MLCP) activity. Ca2+ inﬂux via calcium channels located in the membrane (voltage- operated channel (VOC) and receptor- operated channel (ROC)) and Ca2+ release from intracellular stores in the sarcoplasmic reticulum (SR) via phospholipase C (PLC)- mediated hydrolysis of phosphotidyl inositol bisphosphate, yielding inositol triphosphate (IP3) result in an increase in intracellular Ca2+. The Ca2+ interacts with calmodulin, forming a Ca2+– calmodulin complex which activates MLCK that phosphorylates MLCP, allowing for the close interaction of the actin and myosin ﬁlaments for force generation. Anumber of vasoconstrictors such as the agonists of α- adrenoceptor (α), thromboxane A2 (TXA2), endothelin 1 (ET), etc. stimulate G- protein coupled receptors (GPCRs) that directly open the ROC causing Ca2+ inﬂux, or through the production of second messengers such as IP3 causing release of the stored Ca2+. Contraction can also be mediated in Ca2+- sensitization mechanism. Rho- kinase becomes activated via the activated RhoA protein, which subsequently phosphorylates MLCP, rendering the enzyme inactive and incapable of de- phosphorylating MLC. Endothelium:the intact endothelium may prevent spasm of the vessel by spontaneous (basal) release of a number of endothelium- derived relaxing such as nitric oxide (NO), prostacyclin (PGI2), and endothelium- derived hyperpolarizing factor (EDHF) to balance the vasocontraction and relaxation in arterial grafts. Importantly, when the endothelium is intact, vasoconstrictors not only cause contraction, but also stimulate receptors located on the cellular membrane of endothelium and cause increase of the intracellular calcium concentration that, as second messenger, mediates release of endothelium- derived relaxing factors (NO, PGI2, and EDHF), which through different mechanisms reduce the intracellular calcium concentration in the smooth muscle cell and cause relaxation. 5HT, 5- hydroxytryptamine; α2, α2- adrenoceptors; ACh, acetylcholine; AII, angiotensin II receptors; ATII, angiotensin II; FP, PGF2α receptors; H2, histamine receptors; His, histamine; K+, potassium; M(M2); muscarinic receptors; MO, methoxamine; NE, norepinephrine; PE, phenylephrine; S1D, 5- HT1D receptors; TP, thromboxane- prostanoid receptors.

Reproduced from He GW, Taggart DP:Spasm in Arterial Grafts in Coronary Artery Bypass Grafting Surgery. Ann Thorac Surg 2016 Mar;101(3):1222– 9 with permission from Elsevier.

ET PGF2αTXA2NE 5HT ACh His ATII

Endothelium-dependent vasodilators

30140 Pharmacology toprevent spasm inconduits

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Papaverine

Papaverine is an opioid derivative and a non- specic vasodilator substance, which relaxes blood vessels through multiple mechanisms including inhibition of phosphodiesterase (PDE) and decreasing calcium inux or inhibition of release of intracellularly stored calcium. However, papaverine is not recommended for systemic use. e major concern of the topical use of papaverine is its acidic nature, which may damage endothelial function. In fact, the pH of commercially available papaverine solution is 4.4 at 2.5mmol/ L and pH 4.8 at 30 µmol/ L. Acommon clinical protocol to topically use papaverine is to mix papaverine with blood (intraluminal 1% papaverine in blood), which may reduce its acidity due to the buering eect of blood.

Nitrovasodilators

Organic nitrates (nitrovasodilators) such as nitroglycerine (i.e. glyceryl trinitrate), sodium nitroprusside, or isosorbide dinitrate are widely used in CABG patients. ey release NO, a powerful stimulant for guanylate cyclase which raises cyclic guanosine monophosphate (cGMP) in the smooth muscle cell, subsequently reduces intracellular calcium concentrations, and leads to relaxation.

In general, nitrates are eective in treating established vascular spasm, regardless of the nature of the contraction, but less potent in prevention of vasospasm. Nonetheless, oral nitrates, including long- acting nitrates such as isosorbide mononitrate, are commonly prescribed aer CABG with arterial conduits as they are inexpensive, readily available, and generally well tolerated.

Calciumantagonists

Classical calcium antagonists were three chemically divergent groups— dihydropyridine (e.g. nifedipine), phenylalkylamines (e.g. verapamil), and benzothiazepines (e.g. diltiazem)— and the eect of these drugs on the human ITA was extensively studied. e new generations of these drugs, particularly the new dihydropyridines such as nicardipine, amlodipine, and cilnidipine, have been developed in the past decades and they all have vasodilatory eects in arterial gras. Some of these new generations of calcium antagonists such as amlodipine and cilnidipine may also stimulate the vascular endothelium to release NO that may further enhance their vasorelaxant eect in arterial gras.

As to the systemic use of calcium antagonists, diltiazem or verapamil was traditionally recommended in RA graing for at least 6months. More recently, due to the improvements in atraumatic harvest techniques, prolonged administration of calcium channel blockers may not be as necessary as previously believed, but most surgeons still prescribe either a calcium channel blocker or longacting nitrate for CABG patients when the RA is used. e role of the systemic use of calcium channel antagonists postoperatively on the long- term patency of RA gras needs further investigation.

Phosphodiesteraseinhibitors

As modulators of vascular smooth muscle tone, intracellular cyclic adenosine monophosphate (cAMP) and cGMP are controlled through synthesis by cyclases and through hydrolysis by PDEs that are classied into least ve types. PDE III inhibitors such as amrinone or milrinone are known to inhibit cGMP- inhibitable low Km cAMP PDE. e eect of the PDE III inhibitor milrinone

on the ITA or RA, and the PDE IIIA inhibitor olprinone on the gastroepiploic artery and RA have been shown to effective in producing vasodilation. Moreover, it is known that the vasodilatory eect of milrinone on the ITA is greater than its effect on the RA.

Alpha- adrenoceptorantagonists

Both ITA and RA–  are α- adrenoceptor- predominant arteries. However, the ITA has few α- adrenoceptors whereas the RA has signicant α- adrenoceptor function. is is the rationale to use α- adrenoceptor antagonists such as phenoxybenzamine as antispastic drugs in CABG as eective agents to prevent catecholamine- mediated spasm of RA., However, theoretically, α- adrenoceptor antagonists are only eective in reversing the contraction evoked by α- adrenoceptors, implying that α- adrenoceptor antagonists may only be eective in one specic mechanism of spasm and may be insucient when the spasm is related to other mechanisms, for example, due to other receptor mechanisms or via the L- type calcium channel. e nature of vasoconstriction and spasm is complex and may involve many other vasoconstrictors such as endothelin 1, TXA, and so on. In fact, Conant and colleagues reported that phenoxybenzamine- treated RA failed to respond to noradrenaline but did respond to vasopressin, angiotensin II, endothelin 1, and potassium chloride and therefore calcium channel inhibition alone is insucient to prevent all spasm in the RA.

Potassium channelopeners

Potassium channel openers (KCOs) repolarize or hyperpolarize the cell membrane. ey therefore decrease the opening probability of voltage- dependent L- and T- type calcium channels and restrain agonist- induced calcium release from intracellular sources through inhibition of inositol trisphosphate (IP3) formation, and lower the eciency of calcium as an activator of contractile proteins. KCOs specically targeting ATP- sensitive K+ channels such as aprikalim, and other KCOs have been studied in the human ITA and found to be potent vasodilators, preventing contraction mediated by a number of receptors. KCOs such as nicorandil are available clinically with antianginal eects and, therefore, KCOs may become a clinically useful antispastic drug in arterial gras.

Prostacyclinanalogue

e synthetic analogue of prostacyclin, iloprost, was recommended as an antispastic drug for RA and ITA conduits and was shown to have superior ecacy over diltiazem in preventing RA spasm in the early period; iloprost was also superior to diltiazem in 2- year angiographic patency of RA conduits.

Other vasodilatoragents

Apart from these commonly used pharmacological vasodilators, other vasodilator agents may potentially be developed as antispastic agents for the gras. ese candidate pharmaceuticals include beta- receptor agonists, dopamine receptor agonists, rho- kinase inhibitors, angiotensin receptor antagonists, heme oxygenase 1, C- type natriuretic peptide, TXA antagonists, vascular endothelial growth factor, antiplatelet drugs, - carnitine, botulinum toxin, and

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Calcium channel

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NO- independent soluble guanylate cyclase activator YC- 1 or NOnucleophile adduct diethylamine/ NO.

Combination ofvasodilators

All vasodilators have their own limitations in some aspect because each of them has a specic mechanism(s) to relax vessels. Combinations of these vasodilators may produce a better eect. Some of the possible combinations have been studied in the ITA and RA. For example, as an intraluminal or topical solution for the preparation of the gras, calcium antagonists (verapamil or nicardipine) and nitroglycerine may have a synergistic eect in the ITA and in RA, and may improve the patency rate of RA gras. Even in the critical situation of lethal spasm problems, the combination of nitroglycerine and verapamil has been reported to successfully relieve spasm in arterial gras through intraluminal

Specific Antagonists of

TXA

Agonists

blocker

[Ca

VOC

PGI

]

ROC

TXA

PLC

cAMP

1P3

injection in a life- salvaging procedure. e method has been used successfully by others to relieve coronary spasm as well and is now used in catheterization laboratories for preventing RA spasm with success.

Combination of other vasodilators is also reported. For example, the combination of milrinone and nitroglycerine has more than an additive eect. In addition, other combinations of vasodilators are also reported but their eect in preparation of arterial gras is yet to be established.

Fig. 40.2 illustrates the pharmacological mechanisms of

vasodilators.

ere are various pharmacologically antispastic protocols available in dierent units around the world. Table 40.1 gives a summary of the pharmacological antispastic protocols used in CABG. Some of the protocols were designed based on the pharmacological studies

ET etc

openers

cGK

PKG

GPCR

SGCs

cGMP

Nitrovasodilators

GTP

PDE inhibitors

5’-GMP

RhoA

GTP

Fig.40.2 Schema of molecular mechanisms of smooth muscle contraction and the relaxation. Contraction is the summation of myosin light chain

kinase (MLCK) and myosin light chain phosphatase (MLCP) activity. Ca2+ inﬂux via calcium channels in the membrane (voltage- operated channel (VOC) and receptor- operated channel (ROC)) and Ca2+ release from intracellular stores in the sarcoplasmic reticulum (SR) via phospholipase C (PLC)- mediated hydrolysis of phosphotidyl inositol bisphosphate, yielding inositol triphosphate (IP3) result in an increase in intracellular Ca2+. The Ca2+ interacts with calmodulin, forming a Ca2+– calmodulin complex which activates MLCK that phosphorylates myosin light chain, allowing for force generation. Vasoconstrictors such as the agonists of α- adrenoceptor (α), thromboxane A2 (TXA2), endothelin 1 (ET), etc. stimulate G- protein coupled receptors (GPCRs) directly opening the ROC causing Ca2+ inﬂux, or through the production of second messengers such as IP3 causing release of the stored Ca2+. Contraction can also be mediated in a Ca2+- sensitization mechanism. Rho- kinase becomes activated via the activated RhoA protein, which subsequently phosphorylates MLCP, rendering the enzyme inactive and incapable of de- phosphorylating MLC. Relaxation:relaxation occurs with MLCP dephosphorylating MLC. This can be fulﬁlled through various mechanisms. For example, it can be via blockage of Ca2+ inﬂux by calcium channel blockers (CCB) to decrease the intracellular Ca2+. The antagonists of speciﬁc vasoconstrictors such as the antagonists of α- adrenoceptor, TXA2, ET, etc. inhibit the ROC associated with GPCRs. Nitrovasodilators via releasing nitric oxide (NO) stimulate soluble guanylate cyclases (sGCs), which increase synthesis of cGMP from GTP. Increased cGMP level inhibits VOC and ROC through protein kinase G (PKG) pathways. NO– cGMP also interacts with the rho- kinase pathway via cGMP regulated protein kinases (cGK), interferes with the MLC and phospho- MLC activity, and ﬁnally relaxes the smooth muscle. The rho- kinase inhibitor inhibits rho- kinase pathway and the phosphodiesterase (PDE) inhibitors increase cGMP level via inhibiting cGMP– 5′GMP activity, relaxing the vessel. Potassium channel openers (K+ openers) open the potassium channels such as calcium- sensitive potassium channels (KCa), cause efﬂux of K+, and hyperpolarize the membrane potential (Em). The membrane hyperpolarization decreases intracellular Ca2+ levels by inhibiting Ca2+ inﬂux through VOC and favours the reuptake of Ca2+ into intracellular stores and extrusion of Ca2+ from the cell, resulting in relaxation. Prostacyclin (PGI2) raises cAMP levels in the cytosol and via activation of the protein kinase Apathway leads to relaxation. This schema also shows that each vasodilator relaxes blood vessels in a speciﬁc pathway, although there are some interactions between the pathways. Apossible protocol for relaxation of coronary artery bypass grafts is to combine two vasodilators that relax the vessel in different pathways.

Reproduced from He GW, Taggart DP. Antispastic Management in Arterial Grafts in Coronary Artery Bypass Grafting Surgery. Ann Thorac Surg. 2016 Aug;102(2):659– 68 with permission from Elsevier.

[Ca

Calmodulin

MLCK

Contraction

Phospho-myosin light

chain

Myosin light chain

Relaxation

Rho kinase

Calcium sensitization

MLCP

Rho kinase

inhibitor

40 Pharmacology toprevent spasm inconduits 303

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Table40.1 Summary ofthe antispastic protocols used inarterial grafting inCABG

Authors Topical IMA GEA RA Systemic Postoperative oral

Mills 1989 Papaverine +

Acar 1992 Papaverine + blood + Diltiazem Diltiazem**

Suma 1991 Papaverine +

Dietl 1995 Papaverine + Diltiazem Diltiazem ‘if spasm is noted’

Dregelid1995 Papaverine +

Reyes 1995 Papaverine 60 mg + 60 mL blood + Diltiazem

Sasson 1995 Papaverine +

Bilgen 1996 Papaverine +

Yavuz 2001 Papaverine +

Girard 2004 Papaverine +

Tatoulis 2004 Papaverine + NG Amlodipine**

Bahcivan 2007 Papaverine +

Kiessling 2013 Papaverine

He GW 1994 VG +

He GW 1996 VG +

Esmore 2000 VG + NG

Yoshizaki 2008 VG +

Mussa 2003 Phenoxybenzamine +

Corvera 2003 Phenoxybenzamine +

Gurevitch 1997 Isosorbide dinitrate @ + + +

Shapira 2000 +

Chavanon 1999 NG +

García- Rinaldi 1999 Milrinone +

Halpenny 2001 + Fenoldopam (D1 agonist)

Zabeeda 2001 +

Möllhoff 2002 +

Inokuchi 2004 + Fasudil (through catheter)

Watanabe 2013 Fasudil +

Tabel 2004 + Diltiazem

Nisanoglu 2006 NG +

Yamaguchi 2006 PDE III inhibitor(olprinone) +

He 2008

NG + Nicardipine One calcium antagonist**

Zheng 2012

Ustunsoy 2009 +

Nicardipine* One calcium antagonist**

Milrinone

Iloprost (5days preop)

* Nicardipine is used in a modiﬁed protocol. ** Used according to the availability, the patient condition, and the preference of the cardiologist for 6months or longer. @ Composite arterial grafting was performed.

:The vasodilator is used systemically, usually by intravenous administration. GEA, gastroepiploic artery; IMA , internal mammary (thoracic) artery; NG:nicardipine and nitroglycerine; RA, radial artery; VG:verapamil + nitroglycerine solution. See original source for full details of studies cited. Reproduced from He GW, Taggart DP. Antispastic Management in Arterial Grafts in Coronary Artery Bypass Grafting Surgery. Ann Thorac Surg. 2016 Aug;102(2):659– 68 with

permission from Elsevier.

on gras, as detailed in a recent review. However, other protocols are rather empirical.

Antispastic methods invenousgrafts

is chapter is focused on the pharmacology of arterial gras. ese same principles are also valid in venous gras. In fact, spasm of

the greater saphenous vein has been a recognized problem during harvesting. e vein is almost inevitably spastic when it is dissected if no pharmacological antispastic method is used. e pharmacological solutions used for arterial gras are also used to prevent the spasm of the vein, such as the combination of verapamil and nitroglycerine. Careful surgical technique including gentle manipulation and dilatation of the vein and proper use of antispastic solutions may maximally prevent spasm of venous conduits.

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Conclusion

In summary, pharmacological methods have been developed to prevent or overcome spasm in both arterial and venous gras. Aperfect antispastic protocol should include an advanced atraumatic surgical technique for harvesting gras, particularly to protect the endothelium, and adequate pharmacological methods. All vasodilator drugs relax the vessel in a specic mechanism or mechanisms. erefore, there is presently no ‘perfect’ single vasodilator as the ‘best’ vasodilator to prevent or treat spasm of the arterial gra against all mechanisms of contraction and multiple methods are used clinically at the moment. It is probably wise to use a combination of pharmacological vasodilators targeting dierent mechanisms of spasm in order to obtain the most reliable eect. Acalcium channel blocker such as verapamil or nicardipine combined with a NO- releasing drug such as nitroglycerine used topically on the gras with adequate systemic use of a calcium antagonist when necessary is a reasonable choice in contemporary CABG surgery to overcome spasm.

Acknowledgments

Supported by the National Natural Science Foundation of China (No.

81641017), and Zhejiang Provincial Natural Science Foundation (LY15H020008).

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22. Corvera JS, Morris CD, Budde JM, Velez DA, Puskas JD, Lattouf OM, etal. Pretreatment with phenoxybenzamine attenuates the radial artery’s vasoconstrictor response to alpha- adrenergic stimuli. J orac Cardiovasc Surg. 2003;126(5):1549– 54.

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26. Marinko M, Novakovic A, Nenezic D, Stojanovic I, Milojevic P, Jovic M, etal. Nicorandil directly and cyclic GMP- dependently opens K+ channels in human bypass gras. J Pharmacol Sci. 2015;128(2):59– 64.

40 Pharmacology toprevent spasm inconduits 305

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https://t.me/medicina_free

SECTION 7

Technical aspects ofcoronary artery bypass gra surgery

Section editors:Joseph F.Sabik, III, Stuart J.Head, and Vipin Zamvar

41. Optimal use of instruments for off- pump

coronary artery bypass grafting 309

Bobby Yanagawa, Michael E.Halkos, and John D.Puskas

42. Incisions for coronary revascularization 315

Valavunar A.Subramanian and Nirav C.Patel

43. Cannulation strategies of the aorta for coronary

surgery 319

Sajjad Raza, Khaled Shorbaji, Salil V.Deo, and Joseph F.Sabik, III

44. How to perform a distal coronary

anastomosis 323

David Glineur and Juan B.Grau

45. Composite grafts 327

James Tatoulis and Brian F.Buxton

46. Sequential coronary grafting 333

Juan B.Grau, Jacqueline H.Fortier, and David Glineur

47. Off- pump coronary artery bypass grafting:tips

and tricks 337

Gianluca Torregrossa, David P.Taggart, and John D.Puskas

48. Intraoperative graft assessment with transit- time

ﬂow measurement and epicardial ultrasound 343

Teresa M.Kieser and Gabriele Di Giammarco

49. Minimally invasive direct coronary artery

bypass 349

Volkmar Falk and Sebastian Holinski

50. Robotic coronary artery surgical

revascularization 353

Bob Kiaii, Vincenzo Giambruno, Michael W.A. Chu, Mary Ann C. Wertan, and Francis P. Sutter

51. Hybrid coronary revascularization 359

Michael O.Kayatta, Henry A.Liberman, and Michael E.Halkos

52. Surgical techniques to bypass diffuse coronary

disease 363

Toshihiro Fukui and Shuichiro Takanashi

53. Redo coronary artery bypass grafting 369

Faisal G.Bakaeen and Lars G.Svensson

54. Avoiding stroke during coronary artery bypass

grafting 375

Gil Bolotin, Michael J.Mack, Antonino Di Franco, and John D.Puskas

55. Anaortic coronary artery bypass grafting 381

W. Brent Keeling, Michael E.Halkos, and John D.Puskas

56. Management and impact of preoperative,

intraoperative, and postoperative cardiogenic shock/ cardiac arrest in coronary artery bypass graft patients:the role of circulatory support 385

Roberto Lorusso, Hadi Toeg, Simon Maltais, Scott DeRoo, and Koji Takeda

57. Prevention of mediastinitis 399

Harold L.Lazar

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