Coronary collateral vessels are able to supply blood to a myocardial territory vascularized by severely stenosed or occluded epicardial arteries. They may contribute significantly to the limitation of ischemia and infarct size.^1,2 Improvement in left ventricular function^3,4 and prevention of left ventricular aneurysm formation⁵ also has been attributed to the presence of collateral vessels.

The management of coronary disease in patients with spinal or intracranial disease may be challenging. In some cases, coronary lesions may require treatment before neurosurgery, while in others, myocardial ischemia or infarction may occur in the postoperative patient or simultaneously with stroke or intracranial hemorrhage. Patients with subarachnoid and intracranial hemorrhage have a high incidence of cardiovascular complications,¹ and antiplatelet and anticoagulant medications normally used in coronary disease may further increase the risk of hemorrhage.² Recent neurosurgery is widely considered to be a contraindication to the anticoagulation and antiplatelet therapy necessary for coronary revascularization, and there are no established guidelines for the management of these patients. We present 5 cases of coronary intervention in neurosurgical patients with a discussion of strategies to reduce procedure-related risk.

Technique. Percutaneous transmitral commissurotomy (PTMC) was first described by Inoue et al in 1984 as an alternative to surgical closed mitral commissurotomy for severe rheumatic mitral stenosis (MS).¹ PTMC is less traumatic, cosmetically more acceptable and its early and mid-term results in selected cases are similar or better than surgical commissurotomy. Two techniques have been established for balloon mitral valvotomy: single- (Inoue) and double-balloon.² Both procedures have been shown to produce an improvement in mitral valve area, hemodynamics and functional class.^3–9 In developing countries, cost issues are the major problem in managing rheumatic MS due to the low socioeconomic status of many patients. This problem was addressed by Cribier et al¹⁰ and Arora et al¹¹ with the development of a percutaneous metallic device that can be autoclaved and reused.

An infrequent, but potentially lethal, complication after aortic valve replacement (AVR) is the occurrence of iatrogenic coronary ostial stenosis. This complication has been observed after both mechanical and bioprosthetic valve use and its reported incidence varied between 0.3% and 5%.^1,2 The most likely pathophysiological mechanism proposed is posttraumatic fibrous intimal proliferation caused by coronary ostia cannulation for direct cardioplegia during the operation.² We report a unique case of early occurrence of left main stem (LMS) obstruction 2 weeks after AVR with large thrombotic burden in a patient not receiving any antithrombotic or antiplatelet therapy.

Stent thrombosis (ST) is an important, life-threatening complication of percutaneous coronary intervention (PCI) and coronary stent placement that has been associated with mortality rates of up to 45%.¹ There is currently particular concern regarding the frequency of late ST in PCI patients receiving drug-eluting stents (DES) in whom, despite optimal therapy, the incidence in large “realworld” series remains 0.5–1%.^2,3 The etiology of ST is likely to be multifactorial.⁴ It is well established that there are: (a) procedural risk factors including stent underdeployment,⁵ length of stented segment,⁶ and the presence of residual dissection;⁷ (b) hematological variables such as increased platelet reactivity,⁸ premature discontinuation of or resistance to antiplatelet medication;^9–15 and (c) idiosyncratic factors including a form of hypersensitivity.¹⁶ In additio

Mitral stenosis (MS) is still frequent in many countries where rheumatic fever remains endemic.^1–2 In Western countries, since the disappearance of rheumatic fever, it has become infrequent and remains a clinical entity due to immigration and restenosis after surgical commissurotomy. Percutaneous mitral commissurotomy (PMC), which was introduced more than 20 years ago,³ acts similarly to surgical commissurotomy by splitting the closed commissures (Figure 1). Sometimes the fracturing of calcification may play a role in specific circumstances.

Stroke is the third leading cause of mortality in the developed world.¹ The incidence of first-ever strokes was > 731,000 in 1996 in the United States alone.² In addition, stroke is the leading cause of serious disability and morbidity and has devastating consequences, not only on the functional status of affected patients, but also on their family and caregivers.¹
Atrial fibrillation (AF) is one of the most common cardiac arrhythmias and its association with stroke is well known. Certain therapies are available to reduce the risk of stroke associated with AF. This paper discusses the therapies available to reduce AF-associated stroke risk and focuses on the novel approach of percutaneous left atrial appendage (LAA) exclusion.

Intracoronary brachytherapy using β- or γ-irradiation is effective in reducing angiographic restenosis as well as target vessel revascularization (TVR) in patients with in-stent restenosis (ISR) after bare-metal stent (BMS) implantation.^1–5 Today, however, the technique is rarely used due to important logistic demands, the occurrence of stent-edge restenosis, a certain need for late TVR (“late catch-up phenomenon”), and most importantly, the introduction of drug-eluting stents (DES).⁶ Total occlusion occurring between 6 and 12 months after the index procedure has been identified as a major drawback of brachytherapy.⁷ Most brachytherapy trials^1–5 including the two recently-published randomized comparisons of brachytherapy and DES^8,9 reported follow-up periods of 9–12 months with only a few long-term (i.e., > 1 year) observations.^5,10–16 This may have been

Atrial septal defects (ASD), which comprise roughly 10% of all congenital cardiac disease, are frequently first encountered in the adult population.¹ Significant shunting results in the insidious development of symptoms, culminating in overt heart failure typically in the third to fifth decade of life.^2–4 Despite this typically late presentation, management of these defects has historically centered on the belief that early surgical repair during the asymptomatic period prevents progression, improving both the quality and quantity of life. Indeed, the age of 25 years was initially seen as a cutoff after which a survival benefit from repair may no longer be apparent.⁵ So what then to do with the majority that present later in life, when anatomy and hemodynamics indicate chronic volume overload and patients are almost uniformly symptomatic? Is repair justified and, if so, up to what age?