Although the backup force of a guiding catheter is important for successful percutaneous coronary intervention (PCI), no theory has been proposed thus far regarding the factors involved in its generation. Thus far, our understanding stems only from the opinions of experienced individuals in this field. In this study, we constructed an arterial tree model and measured the backup force of guiding catheters in simulations of transfemoral interventions (TFI) and transradial interventions (TRI). In this paper, we discuss our observations on the important factors that determine the backup force of guiding catheters in the left coronary artery.

Materials and Methods

Reports to the Center for Devices and Radiological Health (CDRH) of the FDA regarding serious injuries and deaths associated with the use of vascular hemostasis devices¹ provided the impetus for this study. These devices are used primarily to stop bleeding from the femoral artery catheterization site following cardiac diagnostic or interventional procedures. The most commonly used hemostasis devices provide two types of mechanisms for percutaneously controlling bleeding, either deploying sutures to close the femoral puncture site or re-absorbable collagen plugs to temporarily seal the arteriotomy, so as to allow the natural hemostatic process to take place.

It was the guiding catheter that prevented the successful clinical launch of percutaneous transluminal coronary angioplasty on March 22, 1976. The patient was afflicted with generalized atherosclerosis. His aorta was completely occluded. Andreas Gruentzig attempted coronary angioplasty to treat end-stage triple vessel coronary artery disease because the patient’s symptoms prevented his mobilization from the intensive care unit, and he had been turned down by the cardiac surgeons. The preliminary dog experiments were carried out with stiff 10 French (Fr) guiding catheters featuring a shape somewhere between a left Judkins catheter and a multipurpose catheter. Using the brachial approach, it proved impossible to cannulate the left main stem, thus the procedure was abandoned. No balloon catheter had been introduced, thus the procedure was not considered to be the first case of coronary angioplasty.

Percutaneous coronary catheterization and revascularization are commonly performed all over the world. Among various access sites for coronary interventions, most cardiologists favor the femoral approach, while the procedure via the radial artery is only performed by a limited number of operators (less than 2% in the United States), probably because of the steep learning curve the radial procedure requires.^1,2 However, it has been shown that the transradial approach to coronary interventions presents a series of advantages that make it an attractive alternative to the brachial or femoral approaches.³

Since the first description of transradial coronary stent implantation in 1993,¹ there has been a rapid increase in the number of coronary diagnostic and interventional procedures using this approach. The radial artery (RA) technique has potential advantages over the procedure done from the femoral artery (FA). These may include a low risk of bleeding complications from the access site, patient comfort, and early mobilization and discharge from the hospital.² It is ideal for obese patients, for patients who are unable to lie flat for more than a short period and for those who require prolonged heparinization or the administration of glycoprotein IIb/IIIa inhibitors.

Percutaneous transluminal coronary angioplasty (PTCA) may be an effective treatment in selected patients with left ventricular dysfunction, but acute and long-term mortality rates are higher than in patients with normal left ventricular function.^1–5 Coronary artery stenting improves procedural success rates and reduces restenosis in patients with normal left ventricular function as compared to angioplasty,^7,8 but in patients with depressed left ventricular ejection fraction (EF), the results of stenting have not been widely reported. The goal of this study was to describe our experience with coronary stenting in patients with a left ventricular EF less than or equal to 40%.

Methods

Intracoronary radiation therapy (IRT) for in-stent restenosis (ISR) in native coronary arteries and saphenous vein grafts (SVG) has substantially reduced the rate of recurrent restenosis compared with conventional percutaneous coronary intervention (PCI).^1–5 However, 20–25% of patients treated with IRT require repeat revascularization to the irradiated site due to restenosis.^6,7 The optimal treatment strategy for these patients remains unclear. Repeat conventional PCI has been shown to be safe but is associated with a high recurrence rate.⁷ Although coronary artery bypass grafting (CABG) may offer a more definitive treatment option, patients may not always be suitable for a repeat surgery that may be associated with high morbidity and mortality rates.

Since the introduction of coronary stenting to interventional cardiology in 1989, improvements in stent implantation techniques and antiplatelet drug therapy have dramatically improved the short-term and long-term outcomes of percutaneous intervention, and stenting is now routinely performed in 90% of all percutaneous coronary interventions (PCI). Coronary stenting was initially approved for treatment of the acute complications of balloon angioplasty: by providing a mechanical scaffold for the vessel wall, sealing dissections and preventing elastic recoil, stents reduce the risk of abrupt vessel closure¹ (Figure 1). As a result, emergency coronary artery bypass graft (CABG) surgery is now required in fewer than 1% of stent procedures compared with 5% of conventional balloon angioplasty procedures.^2,3

While the approach to identifying and treating a high-grade, symptomatic and ischemia-producing coronary stenosis is readily apparent, the optimal treatment of lesions without these characteristics is less established. The uncertainty is because plaque rupture and coronary thrombus development occurs with non-stenotic lesions.¹ Additionally, while it only takes one plaque rupture or erosion to cause myocardial infarction and its attendant consequences, numerous plaques often exist in a single coronary artery, let alone a single patient. These facts have led to increasing interest in identification of the vulnerable plaque.

Background. A number of studies have examined the environmental and genetic basis contributing to the pathogenesis of various disease states. This has been studied in monozygotic twins and recently published. Recent reports have examined disease prevalence, mechanism of onset, and disease progression in large cohorts of twins as it pertains to insulin resistance states,¹ congenital heart disease,² Parkinson’s and other neurologic disease states,³ as well as gastroesophageal reflux disease,⁴ to name just a few. Although endocrine disease is thought to generally fit a multifactorial pattern of transmission, twin studies have clearly established a higher degree of genetic susceptibility.^5–8 Despite this, there remains considerable controversy regarding the relative contribution of environmental factors versus genetic predisposition in a variety of disease states.