**5. Summary**

With increasing numbers of coronary revascularisations taking place globally, the challenges and late complications of percutaneous intervention are also growing. The search

Drug Eluting Balloon 135

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for an ideal device for PTCA is ongoing. The problem of restenosis is very well described as the 'Achilles heel' of coronary intervention. It not only necessitates repeat procedures but also significant symptoms in patients and the treatment is challenging. After the failure of systemic pharmacotherapy, local drug delivery at the coronary lesion site is the current treatment strategy for restenosis and the stent-based platform is the most extensively used. The limitations of DES {Sharma et al, 2010} and problems of late stent thrombosis have shifted the treatment goal from procedural success to keeping the long-term problems minimal.

The concept of DEB originated more than a decade ago but only has come into clinical use recently. Although it showed some initially promising results in animal study and first in man trials, the subsequent studies have failed to demonstrate their superiority over more traditional approaches. DEB certainly seems to offer promise in the treatment of ISR, and possibly in de novo lesions in small coronary vessels. In such scenarios it has several advantages over DES: it helps to avoid the double/triple metal layer which results in making the coronary vasculature into a metal jacket, thereby distorting the anatomy; it potentially provides homogenous drug distribution in the vessel wall, thus reducing the effects of delayed endothelialization of stent struts; it is free of the polymer matrix used in DES, thus removing the stimulus for late thrombosis; advantages are observed despite a shorter period of dual antiplatelet therapy usage, thus probably reducing costs and problems associated with prolonged dual antiplatelet treatment; and may have a role in small, tortuous, heavily calcified coronaries or bifurcation lesions, where DES continues to underperform.

The 2010 European Society of Cardiology Myocardial revascularisation guidelines suggest considering DEB use in treatment of BMS restenosis and for DEB with proven efficacy/safety profile, according to the respective lesion characteristics of the studies {ESC & EACTS, 2010}. Overall the data available so far does not convince us that DEB will replace all DES. Further studies are required in selective lesion subtypes. It is definitely a promising new treatment strategy on the coronary interventionist's shelf.

#### **6. References**


for an ideal device for PTCA is ongoing. The problem of restenosis is very well described as the 'Achilles heel' of coronary intervention. It not only necessitates repeat procedures but also significant symptoms in patients and the treatment is challenging. After the failure of systemic pharmacotherapy, local drug delivery at the coronary lesion site is the current treatment strategy for restenosis and the stent-based platform is the most extensively used. The limitations of DES {Sharma et al, 2010} and problems of late stent thrombosis have shifted the treatment goal from procedural success to keeping the long-term problems

The concept of DEB originated more than a decade ago but only has come into clinical use recently. Although it showed some initially promising results in animal study and first in man trials, the subsequent studies have failed to demonstrate their superiority over more traditional approaches. DEB certainly seems to offer promise in the treatment of ISR, and possibly in de novo lesions in small coronary vessels. In such scenarios it has several advantages over DES: it helps to avoid the double/triple metal layer which results in making the coronary vasculature into a metal jacket, thereby distorting the anatomy; it potentially provides homogenous drug distribution in the vessel wall, thus reducing the effects of delayed endothelialization of stent struts; it is free of the polymer matrix used in DES, thus removing the stimulus for late thrombosis; advantages are observed despite a shorter period of dual antiplatelet therapy usage, thus probably reducing costs and problems associated with prolonged dual antiplatelet treatment; and may have a role in small, tortuous, heavily calcified coronaries or bifurcation lesions, where DES continues to

The 2010 European Society of Cardiology Myocardial revascularisation guidelines suggest considering DEB use in treatment of BMS restenosis and for DEB with proven efficacy/safety profile, according to the respective lesion characteristics of the studies {ESC & EACTS, 2010}. Overall the data available so far does not convince us that DEB will replace all DES. Further studies are required in selective lesion subtypes. It is definitely a

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**7** 

*South Africa* 

**Cardiac Postconditioning: An Additional** 

Following acute myocardial infarction (AMI), early reperfusion therapy with thrombolytic therapy or primary percutaneous coronary intervention therapy (PCI) is the best way to salvage the heart by limiting the infarct size and preserving the left ventricular function. The early survival benefits of reperfusion are probably sustained lifelong and after 20 years, the survival rate of 27% in patients treated with conventional therapy is increased to 37% in patients treated with reperfusion therapy (thrombolytics and/or PCI) (van Domburg *et al.*

However, the benefits of reperfusion come at a price as restoration of the blood flow in the coronary arteries can paradoxically cause myocardial injury. Lethal reperfusion injury manifests itself clinically as stunned myocardium, arrhythmias and endothelial damage (Yellon and Hausenloy 2007). Although still unclear, the mechanisms behind reperfusion injury involve multiple processes including an increase in oxidative stress (Bolli *et al.* 1989), inflammatory damage (Vinten-Johansen 2004), a change in myocyte osmolarity (Garcia-Dorado and Oliveras 1993), calcium loading (Dong *et al.* 2006, Murphy *et al.* 1987) and a

The rapid return of blood in the ischemic myocardium generates an oxidative stress which itself can mediate myocardial injury (Zweier 1988). The release of reactive oxygen species consecutive to the oxidative stress may generate a degree of myocardial injury superior to ischemia alone, partly due to the reduced bioavailability of the potent vasodilator nitric oxide in the vasculature (Zweier and Talukder 2006). The oxidative stress also contributes to the excessive increase of intracellular calcium inducing cardiomyocyte death by hypercontracture and inadequate opening of the mitochondrial permeability transition pore (mPTP) opening (Piper *et al.* 1998). The opening of this pore leads to uncoupled oxidative phosphorylation , depletion of adenosine triphosphate (ATP) and death (Hausenloy and Yellon 2003). Myocardial ischemia causes a progressive decrease in intra- and extra-cellular pH (Inserte *et al.* 2011). At the onset of reperfusion, the removal of extracellular protons and the correction of intracellular acidosis exerts an adverse effect due, in part, to the intracellular sodium and calcium overload (Piper *et al.* 1996). An upregulation of cell

**1. Introduction** 

2005).

**1.1 The concept of lethal reperfusion injury** 

change in pH (figure 1) (Inserte *et al.* 2011).

**Therapy to Limit Cell Death Following** 

*Hatter Cardiovascular Research Institute, University of Cape Town* 

Sandrine Lecour, Lionel Opie and Sarin J. Somers

**Myocardial Infarction** 

