Efficacy of pacing therapies for treating atrial tachyarrhythmias in patients with ventricular arrhythmias receiving a dual-chamber implantable cardioverter defibrillator.

BACKGROUND: Although overdrive pacing for treating atrial flutter is well established, the efficacy of device-based atrial pacing for treating spontaneous atrial tachyarrhythmias in patients with implantable cardioverter defibrillators (ICD) is unknown. This study evaluated the efficacy of novel pacing therapies for treating atrial tachyarrhythmias in patients receiving a dual-chamber ICD to treat ventricular tachyarrhythmias. METHODS AND RESULTS: A Jewel AF ICD was implanted in 537 patients with ventricular arrhythmia who were followed for 11.4+/-8.2 months (74% had a documented history of atrial tachyarrhythmias). The device discriminated atrial tachycardia (AT) from atrial fibrillation (AF) on the basis of cycle length and regularity, and it used 3 different methods of overdrive atrial pacing (Ramp, Burst+, and 50-Hz burst) to treat AT episodes and one method (50-Hz burst) to treat AF episodes. Pacing successfully terminated 59% of 1500 spontaneous AT episodes in 127 patients and 30% of 880 AF episodes in 101 patients (P<0.001). With AT and AF episodes combined, pacing efficacy was 48%. Pacing efficacy was significantly reduced at AT cycle lengths

Sympathetic influences on the native canine coronary collateral circulation.

OBJECTIVE: The aim was to investigate the influence of the sympathetic nervous system on the native collateral circulation in the intact heart. METHODS: Experiments were performed on 10 open chest dogs anaesthetised with alpha chloralose. The left anterior descending coronary artery was cannulated and embolised with 25 microns microspheres. Collateral resistance was determined from measurements of aortic pressure and retrograde flow. Additional haemodynamic measurements included left ventricular pressure and blood flow in the circumflex coronary artery. RESULTS: Coronary embolisation decreased retrograde resistance from 41.5(SEM 6.0) to 20.1(1.9) mm Hg.ml-1.min-1 (P < 0.01). Left stellate stimulation for 60 s (10 Hz) significantly increased circumflex blood flow and decreased circumflex resistance from 2.1(0.3) to 1.6(0.2) mm Hg.ml-1.min-1. Retrograde resistance during sympathetic stimulation decreased from 19.7(1.8) mm Hg.ml-1.min-1 (P < 0.01). Transient occlusion of descending aorta resulted in changes in perfusion pressure and retrograde flow that were similar to those observed during stellate stimulation. Stellate stimulation after beta blockade with timolol (0.1 mg.kg-1) increased circumflex resistance from 1.9(0.2) to 2.3(0.3) mm Hg.ml-1.min-1 (P < 0.01) but did not alter retrograde resistance. CONCLUSIONS: The sympathetic nervous system does not have a direct effect on native coronary collateral vessels. Increased sympathetic input to the heart does not result in a coronary steal phenomenon. The primary determinant of flow and resistance in the native collateral network during sympathetic activation is the arterial perfusion pressure.

Sympathetic influences on electrical and mechanical alternans in the canine heart.

OBJECTIVE: The aim was to investigate the influence of the sympathetic nervous system on the induction of mechanical and electrical alternans in the intact canine heart. METHODS: Experiments were performed on 8 open-chest dogs anesthetized with sodium pentobarbital. A micromanometer-tipped catheter was used to measure left ventricular pressure, dp/dt and the time constant of isovolumic relaxation. Rapid atrial pacing was used to induce alternans and the left stellate ganglion was stimulated electrically to alter sympathetic tone. The longest pacing cycle length that showed a significant alternation in peak systolic pressure was defined as the alternans threshold. Electrical alternans was detected by comparing the ST-T area in the surface ECG (lead II) on alternate beats. RESULTS: The alternans threshold was 305(s.e.m. 10.4) ms under control conditions and decreased to 271(12.1), 225(33.4), and 177(6.2)ms, as the frequency of left stellate stimulation was increased to 1, 2, and 5 Hz, respectively (P < 0.001). Tau and peak -dp/dt began to alternate at the same pacing cycle length as peak +dp/dt and peak systolic pressure. Electrical alternans was only observed during mechanical alternans and the ST-T area of the strong beat was 243(143)% greater than the ST-T area of the weak beat (P < 0.001). Timolol (1 mg.kg-1) blocked the effect of left stellate stimulation (1 and 2 Hz) on mechanical and electrical alternans. CONCLUSIONS: Left sympathetic activation causes a frequency-dependent reduction in the threshold cycle length for global mechanical and electrical alternans. Alternation in relaxation occurs at the same pacing cycle length as does alternation in contraction. Repolarization alternans in the surface ECG appears to reflect underlying mechanical events.

Baroreflex sensitivity assessed by complex demodulation of cardiovascular variability.

We used complex demodulation of cardiac interval and systolic arterial blood pressure oscillations in the low-frequency band (0.04 to 0.14 Hz) to investigate baroreceptor control of heart rate. Baroreflex sensitivity was defined as the instantaneous amplitude of complex-demodulated oscillations in the RR interval divided by the instantaneous amplitude of complex-demodulated oscillations in systolic blood pressure. We evaluated the method using both simulated and actual data obtained from 33 healthy nonsmokers during supine and standing postures. To test the validity and reliability of the method, we compared the mean values of baroreflex sensitivity calculated using complex demodulation with the values obtained using power spectral analysis and sequential analysis of spontaneous variations in blood pressure and RR interval. All three methods applied to the simulated data yielded the same values of baroreceptor sensitivity. Mean values of baroreflex sensitivity assessed by complex demodulation of the actual data were similar to those calculated by both power spectral analysis and sequential analysis (13.9 +/- 5.2 versus 13.7 +/- 6.7 or 14.3 +/- 6.5 ms/mm Hg for supine and 7.3 +/- 2.8 versus 7.0 +/- 3.0 or 7.2 +/- 2.8 ms/mm Hg for standing, respectively). In addition, a significant correlation existed between the values obtained by complex demodulation and power spectral analysis (r = .97, P = .0001) and sequential analysis (r = .98, P = .0001). Furthermore, complex demodulation-derived baroreflex sensitivity fluctuated across time during both the supine and standing postures, and this could not be discerned by power spectral analysis. The results indicate that complex demodulation provides a dynamic assessment of baroreflex sensitivity and may be a useful tool in exploring reflex autonomic control of the cardiovascular system.

Breath pentane and plasma lipid peroxides in ischemic heart disease.

This study examined the relationship between breath pentane and plasma lipid peroxide levels sampled simultaneously in patients with stable angina (n = 17), unstable angina (n = 23), and controls (n = 10). Plasma lipid peroxides were measured in venous blood as the adduct formed between thiobarbituric acid and malondialdehyde (MDA) using high performance liquid chromatography. Pentane was measured in end-expiratory air using gas chromatography. MDA concentrations in stable (1.81 +/- 0.84 mumol/l) and unstable (1.5 +/- 1.23 mumol/l) angina were not different. However, both groups had significantly (p < 0.005) elevated MDA levels compared to controls (0.41 +/- 0.26 mumol/l). Breath pentane was 0.20 +/- 0.12 nmol/l in controls and not different from stable angina (0.26 +/- 0.20 nmol/l) or unstable angina (0.15 +/- 0.07 nmol/l). When the data from all three groups were combined, there was no correlation between pentane and MDA (rho = -0.09, p = 0.54). In five of the unstable angina patients treated with balloon angioplasty, MDA in pulmonary arterial blood rose by 69 +/- 15% (p < 0.01), and breath pentane rose by 73 +/- 20% (p < 0.01) immediately after balloon deflation. One minute after balloon deflation MDA and pentane had returned to preinflation levels. The results suggest that basal levels of pentane are less useful than MDA as an index of lipid peroxidation in patients with coronary artery disease. However, breath pentane appears to be a sensitive index of reperfusion-induced lipid peroxidation.

Continuous fractionated electrical activity after stimulation of the ventricles during the vulnerable period: evidence for local reentry.

Ventricular multiple extrasystoles and fibrillation were induced in open chest dogs by the delivery of either a single electrical pulse or a train of pulses to the right ventricle during the vulnerable period of the cardiac cycle. Bipolar epicardial electrodes delivered current while bipolar plunge electrodes recorded the activation complexes at various distances from the stimulation site. At stimulus intensities below the threshold for multiple ventricular responses, the electrograms recorded from muscle adjacent to the stimulation site showed fragmented activation complexes that lasted considerably longer than the control complexes. At stimulus intensities that evoked multiple ventricular extrasystoles or fibrillation, the fragmented electrical activity became continuous and bridged the diastolic interval between successive ectopic complexes. The continuous fractionated electrical activity that preceded the appearance of multiple extrasystoles and fibrillation was recorded only from electrodes placed within a few millimeters of the stimulating electrodes and could be evoked only by stimulation during the vulnerable period. Disappearance of the fractionated local electrical activity during a run of extrasystoles was followed immediately by the resumption of a normal rhythm. In addition, the fractionated continuous electrical activity that appeared after delivery of a single stimulus during the vulnerable period could be abolished by the delivery of a second stimulus during the protective zone. The presence of continuous local electrical activity before the development of multiple extrasystoles and fibrillation provides strong evidence that the ventricular fibrillation threshold technique operates by producing local reentrant activity.

Mechanism of the effect of bretylium on the ventricular fibrillation threshold in dogs.

Experiments were performed to determine the importance of sympathetic blockade vs a direct myocardial effect as a mechanism for the antifibrillatory action of bretylium. The ventricular fibrillation (VF) threshold was determined in open-chest, anesthetized dogs by scanning the vulnerable period with either a single electrical stimulus (10 ms) or a train of electrical stimuli (14 pulses, 4 ms, 100 Hz). Using the train-of-pulses technique, the VF threshold increased from 6.8 +/- 0.6 mA to 29.7 +/- 6.4 mA 15 minutes after a 10-mg/kg intravenous bolus of bretylium (p less than 0.001, n = 8). There was no further significant change in the train-of-pulses VF threshold at 2 or 4 hours. Beta-adrenergic blockade with timolol (0.2 mg/kg) increased the train-of-pulses VF threshold from 6.7 +/- 1.6 mA to 24.5 +/- 5.2 mA (p less than 0.01 n = 8) and prevented any further significant change in response to bretylium. When single electrical pulses were used to scan the vulnerable period, bretylium at doses of 10 mg/kg (n = 8) and 100 mg/kg (n = 6) did not alter the VF threshold over a 4-hour observation period. The administration of timolol, alone or in combination with bretylium, did not significantly alter the single-pulse VF threshold. The failure of bretylium to alter the single-pulse VF threshold was not dependent on the site of stimulation. Stimulation of the right sympathetic cardiac nerves showed that 15 minutes of bretylium treatment was sufficient to completely inhibit adrenergic neuronal transmission to the myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Digoxin and the susceptibility of the canine heart to countershock-induced arrhythmia.

This study investigated the effects of therapeutic and subtoxic doses of digoxin on the risk of ventricular tachycardia (VT) after graded, transthoracic shocks in anesthetized dogs. A series of direct current shocks (5, 10, 25, 50, 75, 100, 150 and 200 J) was delivered to 33 normal dogs and 6 dogs with a healed (32 +/- 7 days) myocardial infarct (MI). In 10 untreated dogs, the duration of post-shock VT was highly reproducible when 3 separate series of shocks were delivered at 2-hour intervals. In 6 normal dogs treated with oral digoxin (0.5 mg/day for 5 to 7 days), a series of shocks delivered before and during treatment (serum levels 1.5 +/- 0.5 ng/ml) resulted in the same duration of post-shock VT. In 18 normal and 6 dogs with MI, a series of shocks was given before and 90 minutes after a therapeutic dose of digoxin (0.05 mg/kg intravenously). At this dose of digitalis (serum level 2.5 +/- 1.0 ng/ml), there was no difference in the duration of post-shock VT in either normal dogs or dogs with MI. A third series of shocks was given after achieving subtoxic digitalization with additional intravenous digoxin (0.01 mg/kg) every 30 minutes until a premature ventricular stimulus evoked a repetitive ventricular response. The subtoxic doses of digitalis (serum levels 13.9 +/- 4.7 ng/ml) increased the duration of post-shock VT in both normal dogs (100%) and dogs with MI (700%) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac dysrhythmias in the conscious dog after surgically induced autonomic imbalance.

The ventrolateral cardiac nerve in the dog is a primary branch of the left sympathetics and represents a direct neural link between the central nervous system and the heart. Its electric excitation elicits characteristic shifts in pacemaker and tachydysrhythmias related to its explicit innervation of the inferior atrial, atrioventricular (A-V) junctional and ventricular tissues. Total denervation of the canine heart, sparing the ventrolateral cardiac nerve, produced a long-term model in which only these portions of the heart retained their sympathetic innervation. The trained unanesthetized model dog was subjected to severe exercise in order to determine the effects of elevated levels of sympathetic tone upon these important regions of the conduction system. Reproducible tachydysrhythmias were elicited in all six animals completing the regimen of periodic testing over a period of 136 to 378 days after operation. The abnormal rhythms consisted of shifting cardiac pacemakers and supraventricular A-V junctional and ventricular tachycardias with frequent premature systoles. Comparable abnormalities were not observed in a similarly tested sham-operated animal or in dogs with a totally denervated heart. The exercise-induced dysrhythmias gradually disappeared with time, presumably in relation to autonomic reinnervation of the heart. The characteristic patterns of ventrolateral cardiac nerve and upon its presumed influence upon Purkinje fiber and A-V nodal automaticity and temporal dispersion of refractoriness in myocardial tissues.

Ventricular fibrillation during coronary angiography in dogs: the role of calcium-binding additives.

Coronary angiography with Renografin 76 (RG76) occasionally results in ventricular fibrillation (VF). Angiovist 370 (AV370) is a contrast medium similar to RG76 except the calcium-sequestering agents, sodium citrate and EDTA in RG76 have been replaced by calcium EDTA. To determine whether these sequestering agents contribute to contrast medium-induced VF, a comparison was made of the effects of intracoronary injections of RG76, AV370, and saline solutions containing sodium citrate and EDTA (CIT/EDTA) and calcium EDTA (CA EDTA) on myocardial conduction, local QT intervals, and incidence of spontaneous and induced VF in 32 dogs. Four milliliters of RG76 produced a 111 +/- 12-ms increase in local QT intervals, compared with a 73 +/- 8-ms increase with AV370 (p less than 0.001). Spontaneous VF occurred in 12 of 16 six-milliliter injections of RG76, compared with 4 of 16 injections of AV370 (p less than 0.02) An early-cycle premature impulse applied after every fourth beat induced VF in 15 of 16 four-milliliter injections of RG76 compared with 5 of 16 injections of AV370 (p less than 0.01). As the premature beat conducted through the left anterior descending region, conduction slowing and fractionation occurred, which was less with AV370 than with RG76. The CIT/EDTA solution produced a greater increase in QT intervals (77 +/- 5 ms) than the CA EDTA solution (29 +/- 3 ms) or 0.9% saline solution alone (28 +/- 2 ms) (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

The use of programmed electrical stimulation to assess the fibrillatory propensity of ionic and nonionic contrast media.

Coronary angiography occasionally results in ventricular fibrillation. To compare the fibrillatory propensity of conventional ionic and nonionic contrast media, we measured QT intervals and performed programmed electrical stimulation during intracoronary injection of Renografin 76 (R76), Hypaque 76 (H76), and iopamidol (IOP) in 16 open chest dogs. In ten dogs the incidence of ventricular fibrillation following induction of a single premature ventricular beat after every fourth atrial paced beat was 19/20 with R76, 8/20 with H76, and 0/20 with IOP (P less than .001). When two premature beats were induced, the incidence of ventricular fibrillation was 20/20 with R76, 19/20 with H76, and 1/20 with IOP (P less than .001). In six additional dogs, the mean prolongation of the QT interval was 170 +/- 20 msec with R76, 105 +/- 14 msec with H76, and 63 +/- 9 msec with IOP (P less than .001). Thus, programmed electrical stimulation readily induces ventricular fibrillation during intracoronary injection of conventional ionic contrast media. The incidence of ventricular fibrillation parallels the amount of QT interval prolongation produced. H76, which lacks EDTA and sodium citrate, is less fibrillatory than R76. However, the nonionic medium IOP appears far less fibrillatory than either R76 or H76.

Arterial impedance in patients during intraaortic balloon counterpulsation.

BACKGROUND: Symptomatic improvement of a patient's hemodynamic condition during intraaortic balloon counterpulsation (IABC) is considered to result largely from a reduction in afterload. Afterload can be accurately quantified by arterial input impedance measurements. Here we report the effect of IABC on arterial impedance in humans. METHODS: To characterize the effects of IABC on arterial input impedance, impedance measurements were obtained using aortic annulus Doppler flow and pressure from the aortic balloon catheter. Impedance spectra were compared between the cardiac cycles preceding and following the cycle with IABC in 25 patients. RESULTS: Intraaortic balloon counterpulsation increased stroke volume (23%; p = 0.001), reduced myocardial oxygen demand (11%; p = 0.02), and decreased the aortic pressure at the onset of systole (16%; p = 0.001). There was also a decrease in systemic vascular resistance (24%; p = 0.001), characteristic arterial impedance (21%; p = 0.002), and pulse wave reflection (20%; p = 0.006). Linear regression analysis showed that an increase in stroke volume was predicted only by the decrease in systemic vascular resistance (r = -0.81; p = 0.001). CONCLUSIONS: The reduction in systemic vascular resistance appeared to be the major mechanism by which IABC improved cardiac pumping efficiency. This effect may result from the passive distention of the peripheral vascular bed due to the propagation of the balloon-augmented diastolic pressure through the arterial system.

Expired hydrocarbons in patients with acute myocardial infarction.

Pentane and isoprene concentrations were analyzed in single end-expiratory breath samples using gas chromatography. Breath analysis was performed in 15 patients with acute myocardial infarction, 15 patients with stable angina, and 15 healthy control subjects. The two patient groups were well matched for age, sex, smoking habits, hypertension and serum cholesterol levels. There was no significant difference in breath pentane concentration in the acute myocardial infarction group (0.29 +/- 0.03 nmol/l) (mean +/- SEM) compared to the group with stable angina (0.31 +/- 0.03 nmol/l) or the control group (0.36 +/- 0.04 nmol/l). However, breath isoprene concentration was higher (p < 0.01) in the acute myocardial infarction group (11.4 +/- 1.2 nmol/l), compared to both the stable angina group (7.7 +/- 0.5 nmol/l) and the control group (7.1 +/- 1.0 nmol/l). There was no difference in either the pentane or isoprene concentrations between the control group and the group with stable angina. Since pentane is thought to be an index of lipid peroxidation, the results do not support the presence of enhanced lipid peroxidation in acute myocardial infarction in the absence of thrombolytic therapy or primary angioplasty. The mechanism responsible for isoprene elevation in acute myocardial infarction is unknown.

The middle cardiac vein--a novel pathway to reduce the defibrillation threshold.

UNLABELLED: Defibrillation energy requirements of epicardial implantable cardioverter defibrillator systems are generally lower than endovascular systems currently used. The former has the disadvantage of requiring a thoracotomy and so has a greater morbidity and mortality than an endovascular procedure. The middle cardiac vein (MCV) is an epicardial structure that is accessible by a non-thoracotomy approach. This study investigated the merits of ventricular defibrillation from the middle cardiac vein. METHODS AND RESULTS. Defibrillation thresholds (DFT) were measured in 10 anesthetized pigs, weighing 34.5 +/- 44.1 kg (mean 39 kg). An Angeflex electrode (1.7 mm x 50 mm) was introduced via the left external jugular vein to the right ventricular apex. The MCV was identified with standard angiography techniques and a 4080 (Angeion Corp.) defibrillation electrode (1.6 mm x 65 mm) introduced into the vein. An active can was implanted in the left subpectoral region. The defibrillation thresholds (DFT) of the following defibrillation configurations were assessed using a modified four-reversal binary search: RV-->Can, RV + MCV-->Can and MCV-->Can. The DFT's for the three configurations were 15.5 +/- 2.8 J, 10.8 +/- 3.4 J and 13.7 +/- 2.4 J. Analysis of variance showed that the DFT with the RV + MCV combination was significantly less than the RV alone (p < 0.05) CONCLUSIONS: Defibrillation is possible through the MCV and that incorporating an electrode in the MCV with RV-Can configuration can reduce the DFT by 30%.

Increased defibrillation threshold with right-sided active pectoral can.

UNLABELLED: The aim of this study was to identify the optimal position on the chest wall to place an implant able cardioverter defibrillator in a two-electrode system, consisting of a right ventricular electrode and active can. METHODS AND RESULTS: Defibrillation thresholds (DFT) were measured in 10 anaesthetised pigs (weight 33-45 kg). An Angeflextrade mark lead was introduced transvenously to the right ventricular apex. The test-can (43 cc) was implanted submuscularly in each of four locations: left pectoral (LP), right pectoral (RP), left lateral (LL) and apex (A). The sequence in which the four locations were tested was randomized. Ventricular fibrillation (VF) was induced using 60 Hz alternating current. Rectangular biphasic shocks were delivered 10 seconds after VF induction. The DFT was measured using a modified four-reversal binary search. The results of the four configurations were: LP, 14.6+/- 4.0 J; RP, 18.8+/- 4.2 J; LL, 14.7+/- 4.1 J; A, 14.9+/- 3.1 J. Repeated measures analysis of variance showed that the DFT of RP was significantly higher than LP, LL and A (p < 0.05). CONCLUSIONS: Implanting an active can in the RP position increases the DFT by 29% compared to LP, LL and A sites. The can position on the left thorax does not appear to have a significant influence on DFT.

A systematic evaluation of conventional and novel transvenous pathways for defibrillation.

INTRODUCTION: Conventional implantable cardioverter defibrillators employ endocardial (shock) electrodes with a lead located in the right ventricular apex (RV) and a "hot-can" electrode located subcutaneously in the left pectoral region. In the event of a high defibrillation threshold (DFT) a third electrode is frequently employed in the superior vena cava (SVC). We report the comparison of conventional and novel locations of additional electrodes with the RV/Can configuration, in a porcine model. METHOD: In 12 anesthetized pigs (30-45 kg), endocardial defibrillation electrodes were randomized to the following locations: RV/Can, RV/Can + SVC, RV/Can + main pulmonary artery (MPA) and RV/Can + left pulmonary artery wedge position (PAW), RV/Can + high inferior vena cava (HIVC), RV/Can + Low inferior vena cava (LIVC). Ventricular fibrillation (VF) was induced using 60 Hz alternating current. After 10 seconds VF a rectangular biphasic shock was delivered by the ARD9000 (Angeion Corp). The DFT was determined for each configuration using a modified four-reversal binary search. All configurations were compared using a repeated measures analysis of variance (ANOVA) statistical test and the five 3-electrode configurations were compared to the RV/Can position using a Dunnett test. RESULTS: Mean DFTs: RV = 21.5 +/- 4.8 J, SVC = 16.8 +/- 4.7 J (p < 0.05 vs. RV), HIVC = 21.1 +/- 4.7 J (p <. 0.05), LIVC = 19.1 +/- 5.7 J (p <. 0.05 vs. RV), MPA = 16.0 +/- 5.8 J (p < 0.01), PAW = 17.5 +/- 4.6 J (p < 0.05 vs. RV). CONCLUSIONS: Relative to the RV/can configuration the addition of a third electrode in the PA, PAW or SVC significantly reduces the DFT in the pig. The addition of an electrode to the IVC did not significantly reduce the DFT in our model.

Improved hemodynamic, angiographic and functional results after renal artery stenting.

Eighteen patients with severe renal artery atherosclerosis underwent conventional percutaneous transluminal renal angioplasty (PTRA) followed immediately by implantation of an endovascular stent. Hemodynamic measurements showed a baseline trans-stenotic pressure gradient of 78.3 mmHg that was reduced to 14.8 mmHg after PTRA. The post PTRA trans-stenotic pressure gradient was further reduced to 0.86 mmHg after stent placement. The average baseline diameter stenosis of 81.3% was reduced to 43.7% after PTRA and 6.1% after stent placement. Six month angiographic follow-up revealed restenosis in 6/16 patients. In patients treated for chronic renal insufficiency without restenosis the 6 month creatinine was 1.46 mg/dl compared to a pre-procedure creatinine of 2.4 mg/dl. Therefore those patients with renal insufficiency and renal artery stenosis who had long term patency after successful stent implantation showed significant improvement in renal function at six months. Stent implantation also significantly improved acute hemodynamic results and acute angiographic results compared to conventional renal artery angioplasty.

Outcome of percutaneous coronary angioplasty (PTCA) performed in a low-volume institution by low-volume operators, evaluated by means of the one-month major adverse cardiac event rate.

BACKGROUND: Since an inverse relationship between percutaneous coronary angioplasty (PTCA) case-load and in-hospital major adverse cardiac events (MACE) exists, we intended to evaluate the performance of low-volume PTCA operators, during the first year of our interventional program, by applying the more accurate index represented by the MACE rate within the first month. METHODS: The data relative to both the PTCA procedure and the control visit 3-4 weeks later, were retrospectively reviewed. Death, myocardial infarction and need for revascularization were the end-points evaluated, both globally and with respect to the individual operators. RESULTS: During 1999, 61 consecutive patients (53M, 8F; mean age: 59.9+/-10.4 years) were treated by two full-trained operators. Stable angina was the indication in 75% of cases. Comorbidities as diabetes and prior revascularization, were present in 16 and 5% of cases, respectively. Multivessel procedures were performed in 33% of cases, with a total number of lesions of 84 (77% A/B1 type). Stents were implanted in 70% of cases, as a bail-out in 12%. Procedural success rate was 93%. Overall one-month MACE rate was 3.3%, accounted for by 1 in-hospital emergency coronary surgery occurred to operator 1 (3.6% one-month MACE rate) and 1 elective coronary operation performed in a stable patient previously treated by operator 2 (3% one-month MACE rate). CONCLUSIONS: PTCA performed in a low-volume center by low-volume operators is not necessarily associated with a poor outcome, provided that adequate selection of low-risk cases is accomplished. Although only 52% of the Italian centers met in 1999 the recommended volume standards, reaching optimal case-load should anyway be pursued. Some time should however be conceded, provided that close monitoring of one-month MACE rate shows adequate performance of both the institution and the operators.

Current perspectives The diagnosis of acute pulmonary embolism. A review of the literature and current clinical practice.

The optimal approach to the diagnosis of acute pulmonary embolism is still controversial. The poor sensitivity and specificity of most of the clinical manifestations, the suboptimal accuracy of the majority of the laboratory and instrumental examinations and the highly variable local availability of the diagnostic resources, makes it in fact difficult for a univocal strategy to be adopted. Recently published practical guidelines, however, support the use of lung scanning (either ventilation/perfusion or only perfusion) as a first-line imaging test, since this approach allows for a correct diagnosis in most patients, after careful history taking, physical examination and electrocardiogram, chest X-ray and arterial blood gas analysis performance. When lung scanning is non-diagnostic, either serial non-invasive (i.e. ultrasonographic) evaluation of the lower limbs or pulmonary angiography should follow. Growing evidence is accumulating on the use of spiral computed tomography scanning either as an alternative or as a complement to lung scanning, while echocardiography should be reserved for the bedside evaluation of critically ill patients, when more validated techniques are not readily available. The role of plasma D-dimer measurement has yet to be defined, especially in hospitalized patients. In current clinical practice, however, these recommendations seem to be only partially followed. Depending in fact on the different characteristics of the populations examined in the seven available studies reporting on this issue, the use of the different diagnostic techniques appears highly variable. Although a standard diagnostic pathway does not seem applicable to all patients with suspected acute pulmonary embolism, further work is nonetheless needed in order to identify in different patient subsets the diagnostic approach capable of minimizing the use of diagnostic resources while obtaining the greatest amount of information.