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This study was undertaken to assess the haemodynamic effects of the combined infusion of prostacyclin and piroximone, a phosphodiesterase inhibitor, in 18 patients with severe congestive heart failure. Right heart catheterization was performed with a Swan-Ganz thermodilution catheter and arterial blood pressure was monitored using a radial line. After baseline haemodynamic measurements, prostacyclin was administered in all patients at the incremental infusion rate of 2, 4, 6 and 8 and 10 ng. kg. min during 15min each. After recovery of baseline haemodynamics, patients were randomly assigned to the piroximone infusion rate of 5 or 10μg. kg. min or placebo. After 24 h piroximone or placebo infusion, the same prostacyclin protocol was applied. Prostacyclin infusion added to piroximone resulted in a significant improvement in haemodynamics, as compared to the group receiving prostacyclin added to placebo. As compared to the curve observed with the placebo infusion, 10 ng. kg. min prostacyclin infusion resulted in a further increase in cardiac index, by 41 and 38% (P<0·01) at the piroximone-infusion rates of 5 and 10 ng. kg. min, respectively, whereas systemic vascular resistance decreased by 25 and 21%, respectively (P<0·01). Additionally, a further decrease in pulmonary capillary wedge pressure by 13 and 11% (P<0·05) and in pulmonary vascular resistance by 21 and 19% (P<0·05) was observed at the piroximone-infusion rates of 5 and 10μig. Kg. min, respectively. Consequently, stroke work index increased significantly, as compared to the group receiving prostacyclin added to placebo. This haemodynamic improvement occurred without significant changes in heart rate and mean arterial pressure. Thus, this study shows that in patients with severe congestive heart failure, short-term infusion of prostacyclin is safe and has additive haemodynamic effects on phosphodiesterase inhibitors. [ABSTRACT FROM PUBLISHER]

Endocavitary figurations were practised in 26 cases of high risk ventricular tachycardia (VT) for which antiarrhythmics including amiodarone and class I antiarrhythmic agents given alone or in combination proved ineffectiveness. Permanent VT was present in nine patients at the time of the fulguration session: three were moribund, and two were unconscious. Included in the series were 10 cases of arrhythmogenic right ventricular dysplasia, nine patients had chronic VT several months after myocardial infarction, four had a non obstructive cardiomyopathy, two were idiopathic and one came after repair of the right ventricular outflow tract. Fulguration succeeded in preventing VT in the 22 patients who survived the initial period of treatment in association with therapeutic antiarrhythmics, in eight cases. Three of the four early deaths were probably related to imperfections in the technique. Two late deaths were due to spontaneous evolution of the disease. The follow-up period ranges from a minimum of 15 to a maximum of 34 months, with an average follow-up of nearly two years. The success rate of fulguration alone or for patients receiving prophylactic antiarrhythmic drugs is 90%. Ten patients required two sessions or more before VT was brought under control. [ABSTRACT FROM PUBLISHER]

The percutaneous Hemopump showed beneficial effects during coronary angioplasty in 32 high-risk patients with unloading of the left ventricle during ischemia and maintaining cardiac output with mean aortic pressures of 50 mm Hg in case of cardiac arrest (3 patients). High procedure-related morbidity (occlusion of femoral artery in 2 patients; bleeding with need of transfusion in 4 patients) and mortality (4 of 32 patients) rates demonstrate the need for a very careful selection of patients. [ABSTRACT FROM AUTHOR]

Background: The inflammatory marker long pentraxin 3 (PTX3) has been shown to be a strong predictor of 30-day and one-year mortality after acute myocardial infarction. The aim of this study was to evaluate the kinetic profile of PTX3 and its relationship with interleukin 6 (IL-6), high-sensitive C-reactive protein (hs-CRP) and infarct size., Methods: PTX3, IL-6 and hs-CRP were measured at predefined time points, at baseline (before percutaneous coronary intervention (PCI)), at 12 and 72 hours after PCI in 161 patients with first-time ST elevation myocardial infarction (STEMI)., Results: PTX3 and IL-6 levels increased in the early phase , followed by a gradual decrease between 12 and 72 hours. There were statistically significant correlations between PTX3 and IL-6 in general, for all time points and for changes over time (0-72 hours). In a linear mixed model, PTX3 predicted IL-6 ( p  < 0.001). PTX3 is also correlated with hs-CRP in general, and at each time point post PCI, except at baseline. PTX3, IL-6 and hs-CRP were all significantly correlated with infarct size in general, and at the peak time point for maximum troponin I. In addition, there was a modest correlation between IL-6 levels at baseline and infarct size at 72 hours after PCI ( ρ  = 0.23, p  = 0.006)., Conclusions: PTX3 had a similar kinetic profile to IL-6, with an early increase and decline, and was statistically significantly correlated with markers of infarct size in STEMI patients post primary PCI. Baseline levels of IL-6 only predicted infarct size at 72 hours post PCI.

Objectives: We sought to assess risk stratification by using dobutamine stress echocardiography (DSE) in patients with aortic stenosis (AS) and severe left ventricular (LV) dysfunction., Background: Few data are available on risk stratification for valve replacement in patients with AS, LV dysfunction and low transvalvular gradients., Methods: Low-dose DSE was performed in 45 patients (16 women and 29 men; median [quartile range] age in years: 75 [69 to 79]; left ventricular ejection fraction: 0.29 [0.23 to 0.32]; aortic valve area [cm2]: 0.7 [0.5 to 0.8]; mean transaortic gradient [mm Hg]: 26 [21 to 33]). Patients were classified into two groups: group I (n = 32, LV contractile reserve on DSE) and group II (n = 13, no contractile reserve). Valve replacement was performed in 24 and 6 patients in groups I and II, respectively., Results: Perioperative mortality was 8% in group I and 50% in group II (p = 0.014). Survival at five years after the operation was 88% in group I. Compared with medical therapy, valve surgery was associated with better long-term survival in group I (hazard ratio for death [HR-D] 0.13, 95% confidence interval [CI] 0.002 to 0.49) and reduced survival in group II (HR-D 19.6, 95% CI 2.7 to 142). The effect of valve surgery on survival remained significant in both groups after adjustment for age, diabetes, respiratory disease and hypertension. Medical therapy had the same effect in both groups., Conclusions: In patients with AS, LV dysfunction and low transvalvular gradients, contractile reserve on DSE is associated with a low operative risk and good long-term prognosis after valve surgery. In contrast, operative mortality remains high in the absence of contractile reserve.

The effects of frovatriptan and sumatriptan on internal carotid and coronary vascular haemodynamics were investigated and compared in conscious dogs. Frovatriptan and sumatriptan (0.1 - 100 microg kg(-1)) induced a transient increase in external coronary artery diameter (eCOD) of up to 2.9+/-1.2 and 1.8+/-0.6%, respectively (both P:<0.05). This was followed by a prolonged and dose-dependent decrease in eCOD of up to -5.2+/-1.2 and -5.3+/-0.9% (both P:<0.05), with ED(50) values of 86+/-21 and 489+/-113 micromol kg(-1), respectively. In contrast, only a decrease in the external diameter of the internal carotid artery was observed (-6.0+/-0.6 and -6.2+/-1.4%, both P:<0.05, and ED(50) values of 86+/-41 and 493+/-162 micromol kg(-1), respectively). Frovatriptan was thus 5.7 fold more potent than sumatriptan at the level of both large coronary and internal carotid arteries. After endothelium removal by balloon angioplasty in coronary arteries, the initial dilatation induced by the triptans was abolished and delayed constriction enhanced. The selective antagonist for the 5-HT(1B) receptors SB224289 dose-dependently blocked the effects of sumatriptan on large coronary and internal carotid arteries whereas the selective antagonist for the 5-HT(1D) receptors BRL15572 did not affect any of these effects. In conclusion, frovatriptan and sumatriptan initially dilate and subsequently constrict large coronary arteries in the conscious dog, whereas they directly constrict the internal carotid artery. The vascular endothelium modulates the effects of these triptans on large coronary arteries. Finally, 5-HT(1B) but not 5-HT(1D) receptors are primarily involved in canine coronary and internal carotid vasomotor responses to sumatriptan.

Background: Absolute coronary flow velocity reserve (CVR) after stenting may remain abnormal as a result of several different mechanisms. Relative CVR (rCVR=CVR(target)/CVR(reference)) theoretically normalizes for global microcirculatory disturbances and facilitates interpretation of abnormal CVR., Methods and Results: To characterize potential mechanisms of poststent physiology, CVR was measured using a Doppler-tipped angioplasty guidewire in 55 patients before and after angioplasty, after stenting, and in an angiographically normal reference vessel. For the group, the percent diameter stenosis decreased from 75+/-13% to 40+/-18% after angioplasty and to 10+/-9% (all P<0.05) after stent placement. After angioplasty, CVR increased from 1.63+/-0.71 to 1.89+/-0.55 (P<0.05) and after stent placement, to 2.48+/-0.75 (P<0.05 versus pre- and postangioplasty). After angioplasty, rCVR increased from 0.64+/-0.26 to 0.75+/-0.23 and after stent placement to 1.00+/-0.34. In 17 patients with CVR(stent) < or = 2.0, increased basal coronary flow, rather than attenuated hyperemia, was responsible in large part for the lower CVR(stent) compared with patients having CVR(stent) >2.0. In 8 patients with CVR(stent) <2.0, a normal rCVR supported global microvascular disease. The subgroup of 9 patients with CVR(stent) <2.0 and abnormal rCVR (16% of the studied patients) may require a pressure-derived fractional flow reserve to differentiate persistent obstruction from diffuse atherosclerotic disease or microvascular stunning., Conclusions: Although a majority of patients after stenting normalize CVR for the individual circulation (ie, normal CVR or normal rCVR), in those with impaired CVR(stent), the analysis of coronary flow dynamics suggests several different physiological mechanisms. Additional assessment may be required to fully characterize the physiological result for such patients to exclude remediable luminal abnormalities.

Objectives: We sought to evaluate dobutamine stress echocardiography (DSE) for predicting recovery of viable myocardium after revascularization with cineangiography as a gold standard for left ventricular (LV) function. We studied the influence of late vessel reocclusion on regional LV function., Background: Dobutamine stress echocardiography is a well established evaluation method for myocardial viability assessment. In previous studies the reference method for assessing LV recovery was echocardiography, long-term vessel patency has not been systematically addressed., Methods: Sixty-eight patients with a first acute myocardial infarction (AMI) and residual stenosis of the infarct related artery (IRA) underwent DSE (mean +/- standard deviation) 21 +/- 12 days after AMI to evaluate myocardial viability. Revascularization of the IRA was performed in 54 patients by angioplasty (n = 43) or bypass grafting (n = 11). Coronary angiography and LV cineangiography were repeated at four months to assess LV function and IRA patency., Results: Sensitivity and specificity of DSE for predicting myocardial recovery after revascularization were 83% and 82%. In the case of late IRA patency, specificity increased to 95%, whereas sensitivity remained unchanged. In the 16 patients with myocardial viability and late IRA patency, echocardiographic wall motion score index decreased after revascularization from 1.83 +/- 0.15 to 1.36 +/- 0.17 (p = 0.0001), and left ventricular ejection fraction (LVEF) increased from 0.52 +/- 0.06 to 0.57 +/- 0.06 (p = 0.0004), whereas in five patients, reocclusion of the IRA prevented improvement of segmental or global LV function despite initially viable myocardium., Conclusions: Dobutamine stress echocardiography is reliable to predict recovery of viable myocardium after revascularization in postinfarction patients. Late reocclusion of the IRA may prevent LV recovery and influence the accuracy of DSE.

Percutaneous transluminal angioplasty continues to be limited by restenosis. Prevention of restenosis is now focusing on local delivery of therapeutic agents, such as proliferation-inhibiting genes, directly to the site of arterial injury. We evaluated use of the Infiltrator catheter (IVT, San Diego, CA. U.S.A.) for gene delivery within the arterial media. The goals of our study were to evaluate the histologic effects of the injection and the suitability of the Infiltrator catheter for local delivery of viral therapy. We injected the femoral arteries of 21 New Zealand White rabbits. Six animals were used for an evaluation of the intramural distribution of dextran/rhodamine injected via the Infiltrator catheter. In seven animals, injection site histology and in vitro vasoreactivity were studied after an injection of saline. In the remaining eight animals, a replication-deficient adenovirus encoding for the firefly luciferase gene (Ad RSVLuc) was injected, and luciferase activity was quantified 3 and 8 days later. After injection via the Infiltrator catheter, the fluorescent tracer was distributed throughout the entire circumference and width of the arteries. Histologic examination showed minimal damage with partial endothelial abrasion and disruption of the internal elastic lamina confined to the penetration sites. In vitro endothelium-dependent vasodilation was present at a reduced level after injection via the Infiltrator (maximal endothelium-dependent acetylcholine-induced relaxation, 51.5 +/- 7.4% vs. 23.8 +/- 14.6%; p < 0.05). Significant luciferase expression was found in all the arteries, with a significant increase from day 3 to day 8 (5,392.5 +/- 2,300 vs. 2,012 +/- 471 cpm/mg; p < 0.05). These data obtained in a rabbit iliac artery model show that the Infiltrator catheter is an efficient and safe local intramural delivery device that provides significant transgene expression in the arterial wall without causing significant structural damage.

This study attempted to determine whether anatomic findings at angioscopy were associated with adverse early angiographic outcomes following excimer laser-assisted coronary angioplasty. Predictive factors of either coronary abrupt vessel closure or early (< or =24 hours) restenosis after percutaneous coronary angioplasty, including clinical and angiographic variables, have been widely evaluated. The role of angioscopic findings may contribute to identification of patients at risk for early poor outcome. Thirty-seven patients with severe lesions, including 23 total occlusions which underwent successful percutaneous transluminal coronary angioplasty (PTCA) with laser irradiation and adjunctive balloon dilatation (n = 35), or stand alone laser (n = 2), had concomitant angioscopic imaging of the target vessel. All patients had a 24-hour angiographic follow up. Early unfavorable outcome (n = 15) was defined as abrupt vessel closure or restenosis (> or = 50% stenosis) at 24 hours. By multivariate logistic regression analysis, immediate post-PTCA residual percent stenosis was associated with a poor outcome (restenosis: 33 +/- 22% vs no restenosis: 21 +/- 14%, p = 0.05). Angioscopic red thrombus aspect was the most significant correlate for early closure or restenosis (7 of 15 patients with unfavorable outcome vs 2 of 22 patients with favorable outcome, odds ratio, 22.9; p < 0.01) and was associated with a significantly higher early minimal lumen diameter loss (1 +/- 0.8 mm in the presence of a red thrombus vs 0.3 +/- 0.5 mm without thrombus, p < 0.005). Red thrombus appearance is associated with an unfavorable early angiographic outcome in patients who undergo laser-assisted coronary angioplasty.

Background: Abnormal coronary vasomotor responses have been described in transplant patients. The aim of this study was to evaluate the graft epicardial vasomotor responses to different stimuli that increase coronary blood flow., Methods and Results: Twelve heart transplant recipients with angiographically normal epicardial coronary arteries were compared 2.7 +/- 1.2 months after surgery with 6 control subjects. Coronary flow velocity was measured with a guidewire Doppler. Coronary diameter changes of the proximal and midportion of the left anterior descending coronary artery were assessed by quantitative coronary angiography during rapid atrial pacing, cold pressor test, supine exercise, and subselective infusion of papaverine and after intracoronary injection of linsidomine (SIN-1). Catecholamine plasmatic levels were determined at the different stages of the protocol. In 6 other transplant patients, a cold pressor test was performed before and after intracoronary infusion of phentolamine (10 micrograms.kg-1.min-1). Coronary flow velocity increased significantly in both groups during each phase of the protocol. In control subjects, dilation was observed in response to atrial pacing (8.7 +/- 7.6%; P < .05), CPT (8.8 +/- 2.3%; P < .01), exercise (14.5 +/- 9.4%; P < .001), and papaverine infusion (14.2 +/- 6.1%; P < .001) and after injection of SIN-1 (26.8 +/- 11.9%; P < .001). In transplant patients, similar dilation was observed during atrial pacing (8.2 +/- 8.3%; P < .05) and papaverine infusion (14.6 +/- 7.8%; P < .001) and after SIN-1 (25.8 +/- 10.8%; P < .001). CPT and exercise caused slight constriction (-3.5 +/- 4.5% and -2.7 +/- 10.5%, respectively; both P < .001 versus control subjects). Norepinephrine plasmatic levels increased in both groups during CPT and exercise. Slight constriction during the cold pressor test (-4.5 +/- 9.6%) changed to dilation (6.8 +/- 7.0%) after alpha-blockade with phentolamine (P < .001)., Conclusions: These results show that flow-mediated, endothelium-dependent vasodilation is preserved early after trans-plantation. Sympathetic stimulation, which overrides the endothelium-dependent mechanism, can be related to hypersensitivity to catecholamines due to denervation.

We undertook this study to evaluate the importance of redistribution images in thallium 201 single-photon emission computed tomography (Tl-201 SPECT) assessment of myocardial viability after acute myocardial infarction. Stress-redistribution-reinjection Tl-201 SPECT was performed in 55 consecutive patients with recent (within 1 month) acute myocardial infarction. The myocardium was divided into 16 segments and activity assessed visually with a score from 0 to 3 on stress-redistribution and stress-reinjection images. A defect was considered moderate if the stress score was 2 and severe if the stress score was 0 or 1. All moderate defects were considered viable, regardless of score on redistribution or reinjection images. Severe defects were considered viable if they were reversible (improvement of 1 score) on redistribution or reinjection images. Stress-redistribution and stress-reinjection images were visually analyzed and compared in terms of viability classification. On visual analysis, 461 segments (52%) were abnormal. One hundred eleven stress defects were moderate; of these, 28 were reversible on reinjection images only and 15 on redistribution images only. However, all of these segments were viable, regardless of the analysis chosen. Of 350 severe stress defects, 48 were reversible on reinjection and irreversible on redistribution images, and 4 were reversible on redistribution and irreversible on reinjection images. Therefore, in viability assessment, 48 segments were misclassified with stress-redistribution analysis, whereas only 4 segments were misclassified using stress-reinjection analysis. Although the usefulness of Tl-201 reinjection imaging is confirmed, redistribution images seem to be of little interest in post-myocardial infarction viability assessment.

Implantation of the wearable Novacor electrically powered left ventricular assist system was performed on March 16, 1993, in a 44-year-old man hospitalized for an acute episode of myocardial decompensation after a 6-year history of dilated cardiomyopathy. He was rehabilitated fully and became ambulatory, awaiting a suitable cardiac graft for 59 days. He is now back to work, enjoying a normal life. This case illustrates the progress made by miniaturization of the external components of the system. General acceptance of the system and psychological adaptation to the new way of life were remarkable.

If the vasodilation of the epicardial coronary arteries caused by linsidomine (SIN-1), the active metabolite of molsidomine, is well established, few data are available concerning the effects of SIN-1 on the acetylcholine (ACh)-induced vasoconstriction of epicardial coronary arteries. Fourteen patients with mild lesions of the left anterior descending artery (LAD) were studied. Intracoronary blood flow velocity was measured by a Doppler probe placed in the proximal segment of the LAD, and cross-sectional arterial area was assessed by quantitative angiography. After initial hemodynamic parameters were measured, 12 mg papaverine was injected into the left main coronary artery. When hemodynamic parameters returned to baseline values, three increasing concentrations of ACh (5 x 10(-7), 10(-6), and 5 x 10(-6) M) were selectively administered into the LAD in a 3 min period for each concentration. While the infusion of ACh 5 x 10(-6) M was continued, 1 mg SIN-1 was injected as a bolus in the ostium of the left coronary artery. After the injection of papaverine, blood flow increased by 197 +/- 8%, with a trend toward vasoconstriction of the proximal and distal segments of the LAD (p = NS). The ACh injection induced a dose-dependent vasoconstriction, reaching 51 +/- 20% on the distal segment of the LAD at the maximum concentration (p < 0.001). After an initial increase in coronary blood flow of 47 +/- 10 and 28 +/- 11% during the first two concentrations of ACh, respectively, the values decreased after the last injection to the level of baseline values. The infusion of SIN-1 antagonized the ACh-induced vasoconstriction, leading to vasodilation of 7.5 +/- 3% (p < 0.005) and 16 +/- 7% (p < 0.001) of the proximal and distal segments of the LAD, respectively; this was associated with an increase in intracoronary blood flow by 42 +/- 8%. We conclude that intracoronary administration of SIN-1 can antagonize the ACh-induced vasoconstriction of epicardial coronary arteries.

Objectives: This study was designed to evaluate the relation between the velocity of flow propagation and left ventricular relaxation by using color M-mode Doppler echocardiography to analyze flow propagation in the left ventricle., Background: Noninvasive attempts to identify alterations in left ventricular relaxation have been hampered because both the relaxation rate and left atrial filling pressure are the determinants of peak early velocity and filling rate., Methods: Color M-mode velocity data were transferred to a microcomputer and compared with conventional pulsed Doppler data to assess the ability of color M-mode echocardiography to analyze velocity field properties. The velocity of flow propagation was measured as the slope of the flow wave front during early filling in normal subjects (n = 29) and in patients with disease that alters relaxation (dilated cardiomyopathy [n = 31], ischemic cardiomyopathy [n = 8], hypertrophic cardiomyopathy [n = 5], systemic hypertension [n = 22] and aortic valve disease [n = 25]). In nine patients with end-stage dilated cardiomyopathy, echocardiographic and left heart catheterization data were obtained at baseline and during intracoronary dobutamine infusion., Results: Color M-mode and pulsed Doppler echocardiographic data were highly correlated (n = 217, r = 0.94, p less than 0.0001, velocity range 0.2 to 1.5 m/s). The velocity of flow propagation was lower in patients than in normal subjects (0.46 +/- 0.15 vs. 0.84 +/- 0.11 m/s, p less than 0.0001). The decrease was significant in all disease forms with or without left ventricular dilation. The velocity of flow propagation was related to peak early velocity in normal subjects (p less than 0.001) but not in patients. It varied inversely with the isovolumetric relaxation time constant during dobutamine infusion and the two variables were highly correlated (p less than 0.0001)., Conclusions: The velocity of flow propagation during early filling seems to be highly dependent on the left ventricular relaxation rate and could be an important tool in studying diastolic function.

From 1973 to 1989, 66 patients received early surgical repair for acute postinfarction ventricular septal rupture. Mean age was 64 +/- 7 years (range, 45 to 80 years). Ventricular septal rupture occurred soon after acute myocardial infarction (3.4 +/- 4 days), and the first medical treatment occurred 6.7 +/- 7 days after onset of acute myocardial infarction. Three patients had a previous myocardial infarction. The site of the rupture was anterior in 38 patients (57%) and posterior in 28 (43%). Forty-four patients (67%) were in shock at the time of admission. Intraaortic balloon pumping was used preoperatively in 28. Operation was performed at the time of maximal efficacy of medical treatment. The same technique was used in all cases. Associated procedures included coronary bypass grafting in 5 patients and valvar operation in 5. The patients have been carefully followed up for up to 16 years. Hospital mortality was 45% (30 patients) and was cardiac related or due to acute renal failure in 25 patients (83%). No correlation could be revealed between early death and age, sex, preoperative intraaortic balloon pumping, or year of operation. Location of the ventricular septal rupture (early mortality of 57% for posterior versus 37% for anterior ventricular septal rupture) and shock at the time of admission (52% versus 32%) showed a trend toward significance (0.08 less than or equal to p less than 0.10). Response to initial active therapy has a strong predictive value (mortality of 70% in unresponsive patients versus 14% in responders; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

A pilot study was performed to determine the safety and efficacy of coronary pulsed mid-infra-red laser angioplasty. The laser was coupled with a novel 2.0 mm multifiber catheter consisting of 37 optical fibers of 150 microns each arranged concentrically around a 0.018-inch central lumen and a soft leading tapered distal tip to maintain coaxial alignment and position plaque in front of fibers. The laser was operated at 500 millijoules/pulse, 3.5 Hz, and 250 microseconds/pulse. Twenty-three patients with stenosis or occlusion of the left anterior descending or right coronary artery were selected for laser treatment. In three patients the catheter could not be positioned against the obstruction. In the 20 remaining patients laser angioplasty increased the diameter of the lumen from 0.3 +/- 0.3 mm to 1.4 +/- 0.3 mm and reduced the stenosis from 91 +/- 8% to 57 +/- 10%. In three patients "stand-alone" laser treatment was sufficient. In 17 patients balloon dilatation further reduced the stenosis to 20 +/- 18%. In two patients who had previously undergone unsuccessful balloon angioplasty with high inflation pressure, laser angioplasty allowed subsequent successful dilatation with low inflation pressure. There were no deaths, perforations, dissections, or arrhythmias. One patient had abrupt reclosure 24 hours after the procedure. Spasm occurred in four patients, and six patients had chest sensations during laser emission. Thus mid-infra-red pulsed coronary laser angioplasty is safe and effective for recanalization of stenosed and totally occluded arteries. The efficacy may be sufficient for "stand-alone" laser treatment. The technique may improve the efficacy of balloon angioplasty in cases of unsuccessful primary dilatation.

To assess the effects of atrial natriuretic factor (ANF) on cardiac function, synthetic human ANF was infused directly into the left main coronary artery of eight patients with congestive heart failure (CHF) and six subjects with normal left ventricular (LV) function (controls) who underwent cardiac catheterization. ANF infusion at the incremental rates of 60, 125, 400, and 800 ng/min induced a dose-related increase in plasma ANF concentrations in the coronary sinus, from 1,223 +/- 590 to 3,923 +/- 1,123 pg/ml in patients with CHF (p less than 0.01) and from 1,041 +/- 605 to 2,710 +/- 1,741 pg/ml in controls (p less than 0.01). Peripheral plasma ANF concentrations (femoral artery) increased from 538 +/- 278 to 752 +/- 262 pg/ml (p less than 0.01) in patients with CHF and from 193 +/- 63 to 401 +/- 147 pg/ml (p less than 0.01) in controls. The increase in peripheral or coronary sinus plasma ANF concentrations did not differ between patients with CHF and controls. At the three lowest ANF infusion rates, cardiac index (CI), systemic vascular resistance (SVR), and LV contractility assessed by peak positive dP/dt remained unchanged both in patients with CHF and in controls. At the highest ANF infusion rate, CI increased from 2.18 +/- 0.53 to 2.54 +/- 0.49 L/min/m2 (p less than 0.01) and SVR decreased from 14.6 +/- 3.6 to 12.8 +/- 4.5 mm Hg.min/L (p less than 0.01) in patients with CHF. There was no associated change in heart rate (HR), mean arterial blood pressure (MAP), cardiac filling pressures, or peak positive dP/dt.(ABSTRACT TRUNCATED AT 250 WORDS)

Vasodilators usually decrease arterial PO2 in patients with congestive heart failure (CHF) because of alteration in ventilation-perfusion (Va/Q) relationships. The effects of sodium nitroprusside (SNP) and urapidil (U), a new selective alpha 1-receptor antagonist, were investigated in seven patients with CHF. The distribution of ventilation and perfusion was examined using the multiple gas elimination technique. The haemodynamic responses to SNP and U were similar, cardiac index increasing by 25% with SNP and by 31% with U. Despite a similar increase of mixed venous oxygen tension, the arterial PO2 decreased from 11.3 +/- 0.8 to 9.6 +/- 0.6 kPa (p less than 0.01) with SNP but remained unchanged (11.0 +/- 0.9 vs 11.4 +/- 0.8 kPa, NS) with U. SNP and U both increased perfusion to lung units with Va/Q ratios of 0.1 or less with no change in shunt fraction. The fractional perfusion to total low Va/Q ratios (low Va/Q + shunt) was higher with SNP than with U (14.1 +/- 2.6 vs 9.5 +/- 2.3%, p less than 0.01). The results suggest that gas exchange and Va/Q relationships are altered less with U than with SNP in patients with CHF.

Results obtained in the past 3 years in patients referred with acute myocardial infarction (AMI) and cardiogenic shock for a mechanical bridge to urgent transplantation permit one to assess the real impact of the present strategy in clinical practice. Ten patients (mean age = 49) were admitted in serious condition (CI = 1.8 +/- 0.2 L/min/m2, PCWP = 28 +/- 6 mmHg, systolic aortic pressure = 88 +/- 20 mmHg, urine output 11 +/- 20 ml/hr) and were treated by maximal sympathomimetic support and i.v. enoximone. Two had to be implanted with a total artificial heart (TAH) and one with a left ventricular assist device (LVAD) for recurrent fibrillation despite hemodynamic improvement, within 8 hr. Two have received transplants and are living well after 20 months. Seven who initially improved markedly have been listed as urgent transplant candidates: two of these have been successfully transplanted, and three died suddenly after 6, 25, and 45 days, respectively. One has undergone successful coronary surgery. One patient (age 62, diabetic) was secondarily rejected for a transplant and died. This experience clearly shows that despite initial spectacular hemodynamic improvement, which was due to optimized medical management, death rate before transplant because of sudden ventricular fibrillation remains unacceptably high. This should prompt early mechanical support, with less invasive systems, in patients with AMI.

Prophylactic implantation of a Hemopump (Johnson and Johnson, Skillman, NJ) has been evaluated in nine patients selected for high risk coronary angioplasty. They were unstable patients, refractory to maximal pharmacology, with indications for revascularization, but contraindications for surgery such as low ejection fraction and lack of material for bypass. In all, the target lesion was located on the last patent vessel. The pump was inserted under local anesthesia, without any graft. A specially designed occluder permitted avoidance of retrograde bleeding during implantation. The bypass flow ranged from 2.5 to 3.2 L/min, and permitted a rise in cardiac index from 2.05 to 2.55 L/min/m2, with a drop in capillary wedge pressure from 13 (7-18) to 10 (7-13) mmHg. During balloon inflation, no electrocardiographic changes were observed, because only minor ventricular arrhythmias occurred. No significant hemolysis was seen (plasma free hemoglobin less than 10 mg/dl in all) after 2 hr of pumping. The only limitation of the technique appears to be difficulty at the time of implantation from narrow, stenosed, or tortuous iliofemoral arteries (3 patients). This experience strongly supports the benefit of temporary left ventricular Hemopump support in high-risk situations and clearly shows the need for a smaller pump.

Patient selection and optimal timing for implantation are unsettled issues in candidates for a bridge to cardiac transplantation. A prospective evaluation of a strategy based on enoximone (E) given IV, in addition to sympathomimetic drugs, permitting to buy time, and delay by hours or days the decisions, has been performed from 1985 to 1988. Thirty-four patients in cardiogenic shock with hemodynamical criteria for TAH implantation have been included: Cl was 1.8 +/- 0.2 L/min/m2 PCWP 29 +/- 7 mmHg, diuresis less than 20 ml/hr. The protocol permitted to postpone decisions of implantation in 30 cases. The 4 unresponsive patients were implanted immediately with TAH (3) or VAD (1). Three were transplanted, two successfully. For 30, time given permitted discovery of hidden contraindications to transplantation in 17 patients. In 13, indication for transplantation was confirmed and performed in 11 within 6 hrs to 8 days (survival 64%). In two, sudden deterioration led to an unsuccessful TAH implantation. Multifactorial analysis showed that a 50% rise in Cl together with a 50% drop in PCWP, a 50% drop in PVR 30 min after IV E has a high predictive value of survival. These data suggest that enoximone IV bolus given in addition to maximal sympathomimetics to patients in cardiogenic shock reduces by 88% the need for TAH or VAD. It also permits a better selection of the candidates.

Thrombolytic treatment efficacy is greater when the delay between onset of pain and treatment is short. To give treatment before admission to a coronary care unit, responsibility needs to be transferred from cardiologists to other physicians working in mobile care units. We conducted a 2-part feasibility study to investigate this strategy. Part 1 evaluated the diagnostic accuracy of mobile care unit physicians. Results from this study indicate that with regard to the diagnosis of acute myocardial infarction, the risk of a wrong diagnosis is low. Part 2 was a placebo-controlled trial involving 100 patients in which 57 received anisoylated plasminogen streptokinase activator complex (APSAC) (30 U) at home and 43 received placebo at home. Patients receiving placebo at home were reevaluated on arrival in a coronary care unit and received APSAC (30 U) if indicated. The main results were that (1) diagnostic accuracy was good--all patients had an acute coronary syndrome and 97 of 100 patients had myocardial infarction; (2) time gain was approximately 60 minutes; (3) coronary patency rate was 72%; (4) ejection fraction was higher in the prehospital group (56.7%) than in the control group (53.4%), but the difference was not significant; (5) there was no rhythmic or bleeding complication related to the prehospital treatment; (6) 5 patients died from cardiogenic shock--2 between home and hospital and 3 in the hospital (3 received thrombolytic treatment at home and 2 received placebo at home and APSAC in the hospital); and (7) prehospital administration of APSAC did not induce a delay in arrival to the coronary care unit.(ABSTRACT TRUNCATED AT 250 WORDS)

From September 1985 to August 1988, 32 patients were referred from various intensive care units throughout Paris for urgent cardiac transplantation or for a mechanical bridge to transplantation. At time of admission, under maximal sympathomimetic therapy, the cardiac index (CI) was 1.81 +/- 0.26 l/min per m2, the pulmonary capillary wedge pressure (PCWP 31 +/- 7 mmHg), systemic vascular resistances (SVR) 2053 +/- 469 dynes s cm-5. In 25, diuresis was less than 25 ml/h. Five were anuric. Prior to any final decision, a new inotropic agent, enoximone, was infused in addition to previous treatment as a 10 min bolus iv 1.5-2 mg/kg every 8 h. In 3, the situation further deteriorated, leading to a Jarvik 7-70 implantation within 12 h. In 29 however, within 3 h, the Cl increased to 2.69 +/- 0.56 as SVR dropped to 1410 +/- 453 and PCWP to 18 +/- 7. Diuresis increased to more than 100 ml/h in all. This permitted an indepth evaluation of the transplant candidates leading to contraindications to transplantation in 16. Nine patients could be weaned off iv enoximone. Four of these are still living (NYHA class III) with a follow up of 6-17 months. In 11, transplantation was performed within 2 days. Four died within a month, 2 with multiple organ failure. One patient died after 5 months. Six are back to normal life, NYHA class I (follow up 10 months-2.5 years). This protocol suggests that in patients with extreme heart failure, immediate survival may be increased by iv enoximone therapy, permitting a better selection of the recipients, more efficient pre-transplantation intensive care and consequently a decrease in the indications for a temporary mechanical bridge to a staged transplantation.