Seminars in interventional cardiology : SIIC最新文献

Shear stress plays a role in lipid accumulation in primary atherosclerosis and vascular remodelling. We will present applications of a new technique, which enables to quantify shear stress in 3D vessel reconstructions. The method is based on 3D IVUS reconstructions of blood vessels either obtained by IVUS pull back (external iliac artery) or by a combination of angiography and IVUS (curved coronary artery). Distribution of wall thickness of a curved human right coronary artery was such that low wall thickness occurred where shear stress was high, and wall thickness was high where shear stress was low. Consequently, an inverse relationship between shear stress and wall thickness was detected. Although vascular remodelling after PTA in external iliac arteries of atherosclerotic Yucatan pigs was predicted both by acute gain and decrements in shear stress, the decrement in shear stress appeared a better predictor. In conclusion, shear stress appears to play a role in primary atherosclerosis and vascular remodelling after PTA.

Positron emission tomography (PET) allows the non-invasive measurement of absolute myocardial blood flow (ml/min/g of myocardium) in man. This has made possible the measurement of myocardial blood flow and the coronary vasodilator reserve (an index of the ability of the coronary microcirculation to dilate) in healthy volunteers to establish the normal values and ranges of these parameters. This technique allows the assessment of the functional significance of epicardial coronary stenoses as well as the investigation of the function of the coronary microcirculation in patients with and without coronary artery disease.

The coronary collateral circulation is an alternative source of blood supply to a myocardial area jeopardized by the failure of the stenotic or occluded vessel to provide enough blood flow to this region. Until recently, only qualitative or semiqualitative methods have been available for the assessment of the coronary collateral circulation in humans, such as the patient's history of walk-through angina pectoris, the registration of intracoronary ECG signs for myocardial ischaemia or angina pectoris during coronary occlusion, or coronary angiographic classification (score 0-3) of collaterals. Studies of coronary wedge pressure measurements distal of a balloon-occluded coronary artery and the recent advent of ultrathin pressure and Doppler angioplasty guidewires have made it possible to obtain pressure or flow velocity data in remote vascular areas and, thus, to calculate functional variables for coronary collateral flow. Those coronary occlusive pressure- and flow velocity-derived parameters express collateral flow as a fraction of antegrade coronary flow during vessel patency of the collateral-receiving vessel. They are both interchangeable, and they have been validated in comparison to 'traditional' methods and against each other. The possibility of accurately measuring coronary collateral flow indices in humans undergoing coronary balloon angioplasty opens areas of investigation of the pathogenesis, pathophysiology and therapeutic promotion of the collateral circulation previously reserved for exclusively experimental studies. The purpose of this article is to review several clinically available methods for the functional characterization of the coronary collateral circulation.

We present the potentials of a novel method of intracoronary flow visualization and quantification that is based on conventional intravascular ultrasound (IVUS) imaging catheters. The quantification of flow is obtained from analysis of the rate of decorrelation of digitized radiofrequency ultrasound echo signals. Flow information is superimposed on the IVUS image using a colour scale. Integration of the blood velocity components normal to the scan plane permits calculation of the volume flow. Validation using IVUS and electromagnetic (EM) flowmeter recordings were obtained in vivo from instrumented pigs. IVUS flow (IVUS(f)) compared favourably to EM flow (EM(f)): IVUS(f)=1.0 EM(f)+5.72 cc/min, r2=0.98. Clinical results for the first five patients investigated are reported. A Doppler wire was used to measure the flow in four coronary arteries and one renal artery in baseline and hyperaemia conditions. IVUS flow and derived coronary flow reserve (CFR) demonstrated a very good agreement with the data derived from the combination of quantitative angiography and velocity when measured with the Doppler wire (DOP(f)): IVUS(f)=1.01 DOP(f)-20 cc/min, r2=0.90 and IVUS(cfr)=1.03 DOP(cfr)-0.03, r2=0.93. This demonstrates that simultaneous morphological and physiological assessment of coronary or peripheral arteries with one IVUS catheter is feasible. This method should be very useful for the evaluation of intermediate coronary stenoses or the results of revascularization procedures.

Flow-dependent vasodilation has been recognized to play an important role in the perfusion of the myocardium and the occurrence of myocardial ischaemia. In the past few years, the role of the endothelium in the regulation of coronary artery dimensions has gained a lot of attraction. Changes in coronary artery size are caused through the contraction and relaxation of the smooth musculature within the vessel wall. Vasoactive substances released from the endothelium play a crucial role in the regulation of vessel size and coronary vasomotor tone. During physiologic exercise, normal coronary arteries dilate, whereas stenotic arteries constrict. This abnormal behaviour of the stenotic artery has been associated with the occurrence of myocardial ischaemia, and has been thought to be either due to: endothelial dysfunction with reduced release or production of the endothelial derived relaxant factor (EDRF); an increased sympathetic stimulation during exercise; enhanced platelet aggregation with release of thromboxane A2 and serotonin; and/or a passive collapse of the disease-free vessel segment within the stenosis when blood-flow velocity increases during exercise. Thus, a diseased coronary endothelium may have a dramatic effect on the function of the coronary arteries, and may cause or contribute to the occurrence of myocardial ischaemia under high-demand situations, e.g. physical exercise or mental stress. Changes in flow-dependent vasodilation have been described in various disease states, e.g. hypercholesterolaemia, hypertension, diabetes mellitus, but also in valvular heart disease, heart failure and transplantation. Most of these alterations are due to functional changes of the endothelium, but vascular remodelling of the coronary arteries with thickening of the intima and an enlargement of the artery may affect these functional changes importantly.

The introduction of Doppler guide wires has allowed the wide-spread use of Doppler technology in the catheterization laboratory for coronary diagnostics and pathophysiological studies. Doppler-ultrasound-derived measurement of coronary flow velocity serves as a substitute for true volumetric flow measurement. To produce reliable and reproducible flow velocity data, the whole Doppler spectrum should be evaluated. Special attention should be paid to the velocity distribution within the spectrum. A spectral display with strong signals in the high velocity range and a sharply defined envelope are markers for a good positioning of the Doppler wire. Additional security for the optimal positioning can give the recently developed tracking indicator. For reliable CFR determination using average peak velocity at rest and during hyperaemia, changes of the shape of the velocity profile and of the cross-sectional vessel area, as well as the position of the Doppler guide wire, have to be taken into account, otherwise the CFR will be underestimated. To eliminate cross-sectional area changes, the vessel should be pretreated with nitroglycerin.

Following the introduction of a transvenous biatrial electrode configuration and a biphasic waveform for internal atrial defibrillation in patients in 1992, it was realized that the standard principles of efficient defibrillation derived from decades of ventricular defibrillation research would not provide painless atrial defibrillation in conscious patients. Over the last five years extensive experimental studies have addressed the risk of ventricular proarrhythmia from synchronized atrial shocks with reassuring results and the influence of the preceding R-R interval on the safety of atrial shocks has been established. Experimental atrial defibrillation research is now aimed at developing waveforms which are less painful and at exploring hybrid therapies including percutaneous right atrial compartmentalization by catheter ablation prior to atrial defibrillation and attempts at multisite pace-entrainment prior to and immediately following the delivery of perithreshold shocks.

Atrial fibrillation (AF) is a re-entrant rhythm, and patients with AF have intra-atrial conduction abnormalities as evidenced by prolonged P-wave duration, abnormal SAECG of P wave, fragmented atrial electrograms and greater intra-atrial conduction delays in response to APDs. Our previous work has proposed that intra-atrial conduction delays and dispersion of refractoriness during extrastimulus testing are site dependent; high right atrial (HRA) stimulation results in marked prolongation of intra-atrial conduction times and AF, whereas distal coronary sinus (CS) stimulation is associated with minimal conduction delays and absence of AF inducibility. Patients with AF induction during HRA stimulation also manifest non-uniform anisotropic conduction in the region of the posterior triangle of Koch. We postulated that if the posterior triangle of Koch is a critical area for re-entry that initiates AF, then prevention of early activation of the posterior triangle may prohibit AF induction by HRA APDs. Distal CS pacing pre-excites the posterior triangle in relation to HRA activation, therefore a subsequent HRA APD will activate the posterior triangle with a longer coupling interval. AF induction by HRA APDs following HRA pacing is prevented when same HRA APDs follow distal CS pacing. We propose that distal CS pacing eliminates the propensity of HRA extrasystoles to induce AF. This observation may have further clinical applicability in AF prevention.