The guidelines of the European Society of Cardiology strongly support the use of PCI in clinically stable patients with coronary artery disease and angina [1]. But in patients with chronic stable conditions and in the absence of a recent myocardial infarction, PCI does not offer any benefit in terms of death, myocardial infarction or the need for subsequent revascularization compared with conservative medical treatment [2]. Patients with stable coronary artery disease and angina were included in the recently published COURAGE Trial [3]. Patients were randomly assigned to undergo PCI and optimal medical therapy or optimal medical therapy alone. This study showed very clearly, that, as an initial management strategy in patients with stable coronary artery disease and angina, PCI did not reduce the risk of death, myocardial infarction or other major cardiovascular events when added to optimal medical therapy. However, exercise-based cardiac rehabilitation is associated with a 25 % reduction in overall mortality and mortality from cardiovascular causes at 3 years [4].

Indications for revascularization in patients with stable angina or silent ischaemia [1]:

In general PCI is effective at reducing angina in patients with symptomatic coronary artery disease. But in stable patients PCI fails to reduce further cardiac events beyond intensive medical therapy. This should be taken in account, when decision to intervention is made.

Decision-making for PCI is important to optimize the success rate, to safe costs and to prevent complications during the procedure. It is generally accepted that revascularization of a coronary stenosis responsible for reversible ischaemia is justified as it relieves angina complaints and in some situations improves patient outcome [1]. In today’s interventional practice, however, a stenosis not clearly responsible for symptoms is often treated, even if ischaemia cannot be attributed to the lesion and even if it is only of mild or moderate severity. This applies to either a single intermediate stenosis or to an intermediate stenosis found incidentally in a patient undergoing stenting because of a more severe stenosis elsewhere in the coronary arteries.

This approach not evidence based, and it is unnecessarily expensive. It might even be harmful because the risk of peri-procedural myocardial infarction or late stent thrombosis is not negligible, even when drug-eluting stents are used [5]. It is unlikely that stenting a haemodynamically non-significant stenosis will improve complaints, and there is no data suggesting that it will improve patient prognosis. Defining the haemodynamic significance of a stenosis from the angiogram is difficult.

Fractional flow reserve (FFR) is an accurate invasive index to determine in the catheterization laboratory whether an angiographically equivocal stenosis is of functional significance (i.e. responsible for reversible ischaemia) [6]. FFR can be simply and rapidly determined just before the planned intervention or during routine diagnostic catheterization. FFR expresses maximum achievable blood flow to the myocardium supplied by a stenotic artery as a fraction of normal maximum flow. Its normal value is 1.0, and a value of 0.75 identifies stenosis associated with inducible ischaemia with a high diagnostic accuracy. A recent study has suggested that FFR-based decision-making about revascularization of an intermediate coronary stenosis results in an excellent long-term outcome [7].

Antihypertensive medication was continued as administered previously. The pharmacological treatment combination contents candesartan and a thiazide diureticum. Because of drug-eluting stent implantation, dual platelet inhibition with aspirin and clopidogrel was started and continued for a minimum of 12 months. No further recommendation for risk factor modification was given by the interventional cardiologist.

In practice, classification of hypertension and risk assessment should continue to be based on systolic and diastolic blood pressure (Table 8.1). This should be definitely the case for decision concerning the blood pressure threshold and goal for treatment (Fig. 8.4).