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The degree of histoincompatibility that can be tolerated, and the relative importance of matching at individual HLA class I and class II locus in bone marrow transplantation (BMT) has not been established. We hypothesized that matching for HLA-DR may not be more important than matching for HLA-A or HLA-B in selection of a donor for successful BMT. We retrospectively analyzed the outcomes of 248 consecutive pediatric patients who received allogeneic BMT from related donors (RD, n = 119) or unrelated donors (URD, n = 129). HLA-A and HLA-B were serologically matched, and HLA-DRB1 were identical by DNA typing in 69% of donor-recipient pairs. Most patients (89%) had hematologic malignancies; the rest had aplastic anemia or a congenital disorder. One HLA-A antigen mismatch was associated with a decrease in survival (p = 0.003) and a delay in granulocyte engraftment (p = 0.02) in recipients of RD marrow; as well as a decrease in survival (p = 0.02) and the development of severe acute graft-versus-host disease (GVHD) (p = 0.03) in recipients of URD marrow. One HLA-B antigen mismatch was associated with a decrease in the survival (p = 0.05) and the development of severe GVHD (p = 0.0007) in recipients of RD marrow. One HLA-DRB1 allele mismatch was associated only with a decrease in the survival (p = 0.0003) of recipients of RD marrow. Results of this study suggest that disparity in HLA-A and HLA-B antigens may not be better tolerated than disparity in HLA-DR allele in allogeneic BMT. Further studies are warranted to confirm our results.

Reactions of coordinatively unsaturated Ru[N(Ph2PQ)2]2(PPh3) (Q = S (1), Se (2)) with pyridine (py), SO2, and NH3 afford the corresponding 18e adducts Ru[N(Ph2PQ)2]2(PPh3)(L) (Q = S, L = NH3 (5); Q = Se, L = py (3), SO2 (4), NH3 (6)). The molecular structures of complexes 2 and 6 are determined. The geometry around Ru in 2 is pseudo square pyramidal with PPh3 occupying the apical position, while that in 6 is pseudooctahedral with PPh3 and NH3 mutually cis. The Ru-P distances in 2 and 6 are 2.2025(11) and 2.2778(11) A, respectively. The Ru-N bond length in 6 is 2.185(3) A. Treatment of 1 or 2 with substituted hydrazines L or NH2OH yields the respective adducts Ru[N(Ph2PQ)2]2(PPh3)(L) (Q = S, L = NH2NH2 (12), t-BuNHNH2 (14), l-aminopiperidine (C5H10NNH2) (15); Q = Se, L = PhCONHNH2 (7), PhNHNH2 (8), NH2OH (9), t-BuNHNH2 (10), C5H10NNH2 (11), NH2NH2 (13)), which are isolated as mixtures of their trans and cis isomers. The structures of cis-14 and cis-15 are characterized by X-ray crystallography. In both molecular structures, the ruthenium adopts a pseudooctahedral arrangement with PPh3 and hydrazine mutually cis. The Ru-N bond lengths in cis-14.CH2Cl2 and cis-15 are 2.152(3) and 2.101(3) A, respectively. The Ru-N-N bond angles in cis-14.CH2Cl2 and cis-15 are 120.5(4) and 129.0(2) degrees, respectively. Treatment of 1 with hydrazine monohydrate leads to the isolation of yellow 5 and red trans-Ru[N(Ph2PS)2]2(NH3)(H2O) (16), which are characterized by mass spectrometry, 1H NMR spectroscopy, and elemental analyses. The geometry around ruthenium in 16 is pseudooctahedral with the NH3 and H2O ligands mutually trans. The Ru-O and Ru-N bond distances are 2.118(4) and 2.142(6) A, respectively. Oxidation reactions of the above ruthenium hydrazine complexes are also studied.

[PPh4]2[WSe4] reacts with an equivalent of [Ag(MeCN)4][ClO4] in DMF to afford a linear polymeric cluster [[Ph4P][(mu-WSe4)Ag]]n (1). Treatment of cluster 1 with excess La(NO3)3.3H2O in Me2SO solution resulted in the formation of a helical chain polymeric cluster [[La(Me2SO)8][(mu-WSe4)3Ag3]]n (2). Cluster 2 crystallizes in the monoclinic space group P2(1/n) with four formula units in a cell of dimensions a = 12.7642(5) A, b = 24.1725(9) A, c = 19.4012(7) A, and beta = 103.546(11) degrees. Refinement by full-matrix least-squares techniques gave final residuals R = 0.0540 and Rw = 0.1116 for 494 variables and 7593 reflections (Fo(2) > 2.0sigma(Fo(2))). The anion [[(mu-WSe4)3Ag3]]n(3n-) in 2 can be described as a butterfly-type SeWSe3Ag2 basic repeating unit linked through interactions with a Ag atom of one fragment and a Ag atom of another to form an intriguing helical array. The CuCN, KCN, and [Et4N]2[WSe4] reaction system resulted in the formation of a novel three-dimensional cluster [[Et4N]2[(mu4-WSe4)Cu4(CN)4]]n (4) either in DMF/2-picoline or in solid at 80 degrees C. Cluster 4 crystallizes in the orthorhombic space group Fddd with cell constants a = 11.090(2) A, b = 23.206(5) A, c = 23.910(5) A, and Z = 8. Anisotropic refinement with 1510 reflections (Fo(2) > 2.0sigma(Fo(2))) and 82 parameters for all non-hydrogen atoms yielded the values of R = 0.0428 and Rw = 0.0887. The anion structure of 4 is built up from a WSe4Cu4 unit bridged by cyanide ligands to form a three-dimensional cross framework. The air- and moisture-stable polymeric clusters easily decompose into small molecular clusters when treated with ligands such as PPh3 and pyridine (Py). Cluster 2 exhibits both strong optical absorption and an optical self-focusing effect (effective alpha2 = 2.2 x 10(-9) m2.W(-1), n2 = 6.8 x 10(-15) m2.W(-1); examined in a 0.13 mM DMF solution). Cluster 4 shows good photostability in the process of measurement and a large optical limiting effect (the limiting threshold is ca. 0.2 J.cm(-2)).

Interaction of Re(N)L(2) [L = N(PSPh(2))(2)] 1 with (CF(3)CO)(2)O or RCOCl afforded air-sensitive acylimido-Re(V) complexes trans-Re[NC(O)CF(3)](OCOCF(3))L(2) 2 or trans-Re[NC(O)R]ClL(2) (R = CCl(2)H 3, CClH(2) 4, CH(3) 5), respectively. Treatment of 1 with (CX(3)CO)(2)O followed by recrystallization from CH(2)Cl(2)/hexane in air led to the formation of the corresponding parent imido complexes trans-Re(NH)(OCOCX(3))L(2) (X = F 6, Cl 7). The structure of 7 has been characterized by X-ray crystallography. The Re-N, average Re-S, and Re-O distances are 1.664(3), 2.441, and 2.116(3) Å, respectively. Deprotonation of 6 or 7 with Et(3)N gave 1. Recrystallization of 3 from CH(2)Cl(2)/hexane in air resulted in oxo-imido exchange and the isolation of the oxo-Re(V) species trans-Re(O)ClL(2). Treatment of 1 with tosyl anhydride gave trans-Re(NH)(OTs)L(2) (OTs = tosyl) 8. Reaction of [n-Bu(4)N][OsNCl(4)] with KL afforded trans-Os(N)ClL(2) 9, which has been characterized by X-ray crystallography. The Os-N, Os-Cl, and average Os-S bond distances in 9 are 1.64(1), 2.577(4), and 2.429 Å, respectively. Treatment of 10 with (CF(3)CO)(2)O, Ag(CF(3)CO(2)), or CF(3)CO(2)H resulted in chloride substitution and the formation of trans-Os(N)(OCOCF(3))L(2) 10. The Os-N, Os-O, and average Os-S distances in 10 are 1.643(5), 2.271(4), and 2.419 Å, respectively. Treatment of 1 with [Ph(3)C]BF(4) resulted in the isolation of trans-Re(NCPh(3))(F)L(2) 11, presumably via the cationic tritylimido intermediate [Re(NCPh(3))L(2)](+). Reaction of 9 with [Ph(3)C]BF(4) led to chloride abstraction and the formation of five-coordinate [Os(N)L(2)]BF(4) 12. The Os-N and average Os-S distances in 12 are 1.646(5) and 2.364 Å, respectively.

The standard treatment of left main coronary artery (LMCA) disease has been bypass surgery (CABG). Recent reports suggested that stenting of LMCA disease might be feasible. From January 1995 to April 1998, we carried out a prospective study of elective stenting of unprotected LMCA disease to evaluate its immediate and long-term results. Of 61 consecutive patients with unprotected LMCA disease, 6 were excluded. Acute procedural success was 100% for the remaining 55 patients, without any complications such as stent thrombosis, myocardial infarction, CABG, or death. During a mean follow-up of 16.1+/-9.6 months, 11 patients (20%) had symptomatic recurrence, between 2 to 6 months after their procedure. Seven patients underwent CABG, two had repeat intervention, one continued with medical therapy, and one died before planned angiography. There was no late sudden death. Forty-four patients (80%) remained asymptomatic. We conclude that elective stenting may be a safe alternative to CABG in unprotected LMCA disease.

The reaction of Ru(Et(2)dtc)(2)(DMSO)(2) (Et(2)dtc = N,N-diethyldithiocarbamate; DMSO = dimethyl sulfoxide) with t-BuNC gave trans-Ru(Et(2)dtc)(2)(CN-t-Bu)(2), 1. Complex 1 crystallizes in the monoclinic space group P2(1)/n with a = 9.753(2) Å, b = 11.583(2) Å, c = 12.974(2) Å, and beta = 91.8(2) degrees for Z = 2. The crystal structure of 1 shows the trans disposition of the two isocyanides; the mean Ru-S and Ru-C distances are 2.409 and 1.977(2) Å, respectively. Treatment of [Ru(diene)Cl(2)](n)() with Na(Et(2)dtc) afforded Ru(Et(2)dtc)(2)(diene) (diene = bicyclo[2.2.1]hepta-2,5-diene (NBD), 2, 1,5-cyclooctadiene (COD), 3). Complex 2 crystallizes in the triclinic space group P&onemacr; with a = 7.316(1) Å, b = 10.346(1) Å, c = 15.123(2) Å, alpha = 103.69(2) degrees, beta = 93.54(2) degrees, and gamma = 100.61(2) degrees for Z = 2. The mean Ru-S and Ru-C distances in 2 are 2.416 and 2.137 Å, respectively. The reaction of cis-Ru(Et(2)dtc)(2)(CO)(2) with iodine gave the 2:1 molecular iodine complex cis-Ru(Et(2)dtc)(2)(CO)(2).(1)/(2)I(2) 4, which crystallizes in the monoclinic space group P2(1)/c with a = 7.347(2), b = 22.227(2) Å, c = 12.891(2) Å, and beta =95.98 (2) degrees for Z = 4. The mean Ru-S and Ru-C and the I-I distances in complex 4 are 2.427, 1.903, and 2.745(1) Å, respectively. Treatment of Ru(Et(2)dtc)(2)(DMSO)(2) with I(2) gave the linear Ru(II)-Ru(III)-Ru(III) trimer [Ru(3)(Et(2)dtc)(6)(DMSO)(2)](I(3))(2), 5, which crystallizes in the triclinic space group P&onemacr; with a = 14.125(3) Å, b = 20.829(6) Å, c = 13.658(3) Å, alpha = 97.57(2) degrees, beta = 110.01(2) degrees, and gamma = 71.25(2) degrees for Z = 2. The structure of complex 6 can be viewed as consisting of a {Ru(2)(III)(Et(2)dtc)(4)}(2+) core and a {Ru(II)(Et(2)dtc)(2)(DMSO)(2)} moiety, which are linked together via the two dithiocarbamate sulfurs of the latter. While the two Ru(III) centers are connected by a Ru-Ru single bond (Ru-Ru = 2.826(2) Å), there is no direct interaction between the Ru(III) and Ru(II) centers. Oxidation of Ru(Et(2)dtc)(2)L(2) (L = PPh(3), t-BuNC) by I(2) gave the respective [Ru(Et(2)dtc)(2)L(2)](+) cations. The reaction of cis-Ru(Et(2)dtc)(2)(PPh(3))(2) with excess tosyl azide gave the diamagnetic Ru(IV) tetrazene complex Ru(Et(2)dtc)(2)(Ts(2)N(4)), 7. Complex 7 crystallizes in the triclinic space group P&onemacr; with a = 10.380(1) Å, b = 11.322(1) Å, c = 15.310(1) Å, alpha = 106.84(2) degrees, beta = 106.87(2) degrees, and gamma = 92.63(2) degrees for Z = 2. The Ru-S and Ru-N(alpha) distances in 7 are 2.385 and 1.98 Å, respectively. The formal potentials of the Ru dithiocarbamate complexes were determined by cyclic voltammetry.

The AVE Micro coronary stent is a balloon-expandable stent with a design that is different from the commonly used slotted tubular or coil stents. The stent delivery system is low in profile and very trackable so that it can negotiate tortuous vessels to reach distal lesions. It also can pass through proximally deployed stents easily. Its moderate radioopacity allows precise stent placement. However, as illustrated in the three case reports presented here, the stent struts did not seem to be firmly embedded into the arterial wall after initial deployment, so that stent migration occurred during subsequent passage of a balloon into the stent for poststenting high pressure balloon dilatation. This new phenomenon of stent migration has not been reported previously with other stents.

Objectives: The aim of this study was to evaluate, using quantitative arteriography, whether the diameter of visually normal coronary segments might be influenced by the relative proximity of visually apparent disease., Background: Severity of coronary artery lesions is commonly referenced against a presumed normal nearby coronary segment with the presumption that visually smooth segments are relatively free of atherosclerotic disease., Methods: Angiograms from 136 male patients with focal coronary disease were examined, and visually normal segments in the proximal portions of the major vessels were identified for measurement of mean segment diameters. Normal segments with immediately adjacent disease were compared with normal segments with distal disease in the same vessel and compared with normal segments in vessels for which the only other visible disease was in distant vessels. Angiograms with entirely normal findings from 26 age-matched men with atypical chest pain were used as controls. Segments were measured after nitroglycerin administration by means of computer-assisted quantitation., Results: Mean diameters of visually normal segments with distant disease were smaller than those of control segments (p < 0.05). Normal left main and proximal left anterior descending coronary artery segments in patients with disease within the same vessel were significantly smaller than normal segments in patients with distant disease (p < 0.05). Normal segments with immediately adjacent disease had smaller mean diameters than normal segments with distal disease in the same vessel (p < 0.05)., Conclusions: Visually normal coronary segments have progressively smaller lumen diameters, depending on the relative proximity of visible disease. Measurement of percent stenosis on the basis of the diameter of apparently normal adjacent reference segments can result in underestimation of coronary lesion severity.

Central venous oxygen saturation (SvO2) closely reflects cardiac output and tissue oxygen consumption. In the absence of an adequate chronotropic response during exercise, SvO2 will decrease and the extent of desaturation may be used as a parameter for rate adaptive cardiac pacing. Eight patients with sinoatrial disease received a DDDR pacemaker capable of DDDR pacing by sensing either SvO2 or piezoelectric detected body movement. Both sensors were programmed to attain a rate of about 100 beats/min during walking, and with the lower and upper rates set at 50% and 90% of age predicted maximum, respectively. Chronotropic behavior of the two sensors were compared in the DDD mode with measurement of sensor responses, during everyday activities (walking, stair climbing, postural changes, and physiological stresses) and at each quartile of workload during a continuous treadmill exercise test. During walking at 2.5 mph, both sensors showed no significant difference in delay time (both react within 15 secs) or half-time (SvO2 = 36 +/- 12 sec and activity 24 +/- 3 sec; P = NS), although SvO2 driven pacing achieved 90% target rate response slower than activity sensing (124 +/- 16 sec vs 77 +/- 10 sec; P < 0.02). SvO2 pacing was associated with a more physiological rate response during walking upslope (68 +/- 12 beats/min vs 57 +/- 10 beats/min; P < 0.05), ascending stairs (59 +/- 10 beats/min vs 31 +/- 6 beats/min; P < 0.05), and standing (34 +/- 7 beats/min vs 9 +/- 2 beats/min; P < 0.05). The SvO2 sensor significantly overpaced in the first quartile of exercise (51.8 +/- 25.6% in excess of heart rate expected from workload), but the rate was within 20% of expected for the remainder of exercise. "Underpacing" was observed with the activity sensor at the higher workload. In conclusion, the SvO2 sensor demonstrated a more physiological response to activities of daily living compared with the activity sensor. Using a quantitative method, the speed of onset of rate response of the SvO2 sensor was comparable to activity sensing, and was more proportional in rate response. Significant overpacing occurs at the beginning of exercise during SvO2 driven pacing, which may be improved with the use of a curvilinear algorithm.

An atrial-based pacing mode is superior to ventricular constant rate demand pacing (VVI) mode in patients with sick sinus syndrome (SSS) by providing both rate adaptation and atrioventricular (AV) synchrony. The use of a non-atrial sensor to overcome chronotropic incompetence and preserve normal intrinsic AV conduction in pacemaker therapy for SSS was investigated in 15 consecutive patients (mean age 66 +/- 2 years). All had intact AV conduction (antegrade conduction capacity > 100 beats.min-1 and an atrial paced to intrinsic R interval of < or = 220 ms). DDDR pacemakers capable of being programmed into atrial rate adaptive (AAIR), dual chamber rate adaptive (DDDR) and ventricular rate adaptive (VVIR) modes were used. Beginning with an acute study, arterial pressure was invasively assessed in each pacing mode during physiological stresses and low level exercise. In the ambulatory phase, the incidence of ventricular pacing and arrhythmias (Holter recording), diurnal blood pressure changes (ambulatory blood pressure recording), and symptom and quality of life level (questionnaires and interviews) were compared. Despite similar heart rate changes during acute physiological stresses, a higher blood pressure was recorded during AAIR or DDDR pacing compared with VVIR pacing. Systolic blood pressure over 24 h was lower in the VVIR mode (122 +/- 5 mmHg) than AAIR/DDDR pacing (129 +/- 6/128 +/- 6 mmHg, P < 0.05). VVIR pacing was associated with a higher frequency of atrial and ventricular ectopics, with two patients developing paroxysmal atrial fibrillation. Ventricular pacing was used in a higher percentage in the DDDR compared with the VVIR mode (64 +/- 11 and 39 +/- 7%, P < 0.03). VVIR pacing was associated with more palpitations, a lower level of general well being and depression. Despite the use of a sensor to overcome chronotropic incompetence, VVIR pacing is a less satisfactory pacing mode for SSS. Although AAIR/DDDR pacing may achieve similar haemodynamic and clinical status, in patients with intact AV conduction, AAIR pacing may be preferable by avoiding an abnormal ventricular activation pattern.

Optimal function of a single lead P wave synchronous rate adaptive ventricular pacing system (VDDR) requires reliable P wave sensing over time and during daily activities. The stability of P wave sensing and the incidence of sensitivity reprogramming in a single pass lead with a diagonally arranged bipole was assessed in 30 patients with complete atrioventricular block over a follow-up period of 12 +/- 1 months (range 6 months to 3 years). Atrial sensing was assessed during clinic visits, by physical maneuvers (postural changes, breathing, Valsalva maneuver, walking and isometric exercise), maximum treadmill exercise and Holter recordings. P wave amplitude at implantation was 1.21 +/- 0.09 (0.5-3.6) mV, and the atrial sensing threshold remained stable over the entire period of follow-up. Using an atrial sensitivity based on twice the sensing threshold at 1 month, P wave undersensing was found in 2, 4, 3, and 7 patients during clinic visit, physical maneuvers, exercise, and Holter recordings, respectively. Atrial sensitivity reprogramming was performed in three patients based on the correction of undersensing during physical maneuvers. Although eight patients had atrial undersensing on Holter recordings, the number of undersensed P waves was small (total 101 beats or 0.013% +/- 0.001% of total ventricular beats) and no patient was symptomatic. One patient had intermittent atrial undersensing at the highest sensitivity, but the VDDR mode was still functional most of the time. No patient had myopotential interference at the programmed sensitivity. One patient developed chronic atrial fibrillation and was programmed to the VVIR mode. Thus, single lead VDDR pacing is a stable pacing mode in 97% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Endocardial P wave amplitude (PWA) is an important determinant of the atrial sensing capabilities of an atrial-based pacing system. Although changes in PWA during physical activities are known to occur in DDD/R pacing, there is little information on the P wave stability in single pass lead VDD/R pacemakers using floating P wave sensing. We investigated the variation of PWA during daily life activities using telemetry recorded atrial electrograms in 21 patients with DDDR pacemakers (Relay or Elite) and 29 patients with single lead VDD/R pacemakers (Unity or Thera). Physical activities resulted in marked individual variability of PWA but, as a group, there was no significant difference between PWA during sitting, standing, lying down, and coughing in both DDDR and VDD/R pacing. In the Elite II pacemaker, walking at 2 miles per hour resulted in significant reduction of PWA (11.6% compared with sitting, P < 0.05). The most consistent reduction in PWA occurred in the relaxation phase of the Valsalva maneuver (VM), with all pacemakers showing a reduction in PWA (mean reduction in PWA compared with sitting in DDDR and VDD/R were 16.6% and 12.8%, respectively). Two patients with DDDR pacemakers (Relay) and three patients with VDD/R pacemakers (1 Unity and 2 Thera) had atrial sensing failure during VM or walking. In conclusion, large variation in PWA occurs during daily life activities. The extent of variation is dependent on the patients, types of atrial lead, and the maneuvers performed. A twice sensing threshold may be insufficient to ensure adequate atrial sensing during these activities.(ABSTRACT TRUNCATED AT 250 WORDS)

Although multisensor pacing may mitigate the inadequacy of rate adaptation in a single sensor system, the clinical role of multisensor driven rate adaptive pacing remains unclear. The cardiopulmonary performance of six patients (mean age 63.5 +/- 10 years) who had undergone the implant of combined QT and activity VVIR (Topaz) pacemakers was assessed during submaximal and maximal treadmill exercise with the rate response sensor randomly programmed to either single sensor mode, QT and activity (ACT), or dual sensor mode, with equal contribution of QT and ACT (QT = ACT). The rate of response, the proportionality, oxygen kinetics, and maximal exercise performance of the various sensor modes during exercise were measured and compared. The ACT sensor mode "overpaced" and the QT and QT = ACT sensor modes "underpaced" during the first three quartiles of exercise (P < 0.05). The ACT sensor mode also gave the fastest rate of response with the shortest delay (13 +/- 1.5 sec vs 145 +/- 58 sec and 41 +/- 17 sec, P < 0.05), time to 50% rate response (39 +/- 2.7 sec vs 275 +/- 48 sec and 203 +/- 40 sec, P < 0.05), and time to 90% of rate response (107 +/- 21 sec vs 375 +/- 34 sec and 347 +/- 34 sec, P < 0.05) and a smaller oxygen debt (0.87 +/- 0.16 L vs 1.10 +/- 0.2 L and 1.07 +/- 0.18 L, P < 0.05) compared to the QT and QT = ACT sensor modes, respectively. These differences were most significant at low exercise workloads. Thus, different sensor combinations result in different rate response profiles and oxygen delivery, especially during low level exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Rapid ventricular tracking response to supraventricular tachyarrhythmia is one major limitation to DDD pacing. In a DDDR pacemaker, sensor-based algorithms have been used to control these arrhythmias. These include the use of an interim rate limit (conditional ventricular tracking limit) or a separate maximum tracking and sensor rate limits (discrepant upper rate). These algorithms limit inappropriate ventricular pacing rate during tracking of pathological supraventricular tachyarrhythmia and atrial flutter by Wenckebach-like prolongation of the AV interval. We observed that this may cause an unexpected extension of the AV interval in patients with high atrial rate and intact AV nodal conduction. This was due to P wave rate above the conditional ventricular tracking limit or maximum tracking limit, but AV paced interval prolongation was avoided by the occurrence of intrinsic conduction, albeit at an AV interval longer than the programmed AV interval. This might appear as failure of ventricular pacing on the ECG. This phenomenon is a modified form of "upper rate" behavior occurring in the AV interval, and should be recognized as a normal behavior rather than pacemaker malfunction.

Objectives: This study evaluated the coronary vasomotor response after successful angioplasty of chronic total coronary occlusions and tested the hypothesis that the degree of distal vasoconstriction is dependent on the change in perfusion pressure., Background: Although distal coronary vasoconstriction has been observed to occur frequently after successful percutaneous transluminal coronary angioplasty, little is known about this vasomotor response after angioplasty of chronic total occlusions., Methods: Thirty patients with successful angioplasty of chronic total occlusions of the left coronary artery were studied. Quantitative coronary measurements were made at 0, 15 and 30 min after angioplasty and again after intracoronary nitroglycerin administration in coronary artery segments distal to the dilated lesion and in a control vessel. The change in distal perfusion pressure was defined as mean systemic arterial pressure minus residual mean trans-stenotic pressure gradient minus mean coronary wedge pressure., Results: The distal segments showed greater vasoconstriction (vs. nitroglycerin) at 15 and 30 min compared with that at 0 min after angioplasty (32.3 +/- 2.2% and 35.2 +/- 2.5% vs. 12.5 +/- 1.8%, respectively, p < 0.005) and compared with control segments (32.3 +/- 2.2% vs. 12.1 +/- 2.0%, p < 0.005, and 35.2 +/- 2.5% vs. 12.5 +/- 2.0%, p < 0.005, respectively). The degree of vasoconstriction at 30 min in the distal segments was found to correlate closely with the change in distal perfusion pressure (r = 0.73, p < 0.001)., Conclusions: Coronary distal vasoconstriction occurs frequently after successful angioplasty of chronic total occlusions and correlates closely with the change in coronary perfusion pressure. These findings support the hypothesis of reset epicardial coronary autoregulation in chronic hypoperfusion such that restoration of normal perfusion pressure after successful angioplasty may provoke reflex vasoconstriction.

Since hypercholesterolaemia is associated with impaired endothelium-dependent vasodilation, a study was conducted to find out whether cholesterol reduction will improve endothelial function in patients with hypercholesterolaemia and normal coronary arteries. 25 men (mean age 51 [SD 8] years) with total serum cholesterol > 6.2 mmol/L) and angiographically normal coronary arteries had their coronary vasomotor responses to intracoronary acetylcholine and nitroglycerin assessed by computer-assisted quantitative angiography at baseline and after 6 months of cholesterol-reducing diet and cholestyramine. Between baseline and follow-up mean total serum cholesterol level fell by 28.7 (SD 5.6)% (p < 0.001); mean low-density lipoprotein (LDL) cholesterol level by 35.6 (8.7)% (p < 0.001); and mean total cholesterol to high-density lipoprotein (HDL) cholesterol ratio by 29.4 (10.6)% (p < 0.001). Acetylcholine significantly reduced the mean segment diameter at baseline, by 21.7 (14.0)% (p < 0.01), but it increased the diameter at follow-up, by 6.16 (13.3)% (p < 0.01), the difference between the two occasions being significant (p < 0.001). Nitroglycerin significantly increased the mean segment diameter, both at baseline, by 18.7 (11.5)% (p < 0.01), and at follow-up, by 19.3 (12.1)% (p < 0.01), the difference between the two responses being not significant. At baseline total cholesterol and LDL cholesterol did not correlate with acetylcholine response, but they did at follow-up (total cholesterol, r = 0.67, p < 0.01; LDL cholesterol, r = 0.64, p < 0.01). Impairment of endothelium-dependent (acetylcholine-induced) dilation of the epicardial coronary arteries in hypercholesterolaemic patients with angiographically normal coronary arteries is thus reversible by reducing serum cholesterol. In addition, the degree of impairment of acetylcholine-induced vasomotor response is related to the cholesterol concentrations after therapy.

PTCA is now applied to patients with unstable acute ischemic syndromes, severe multivessel coronary artery disease, and impaired left ventricular function. To minimize the risk during angioplasty, several coronary and systemic circulation support approaches have been developed as adjuncts to high-risk angioplasty. Local coronary support techniques include the perfusion balloon catheter, the coronary stent, directional coronary atherectomy, laser balloon angioplasty, perfluorocarbon coronary perfusion, coronary sinus retroperfusion, and distal coronary hemoperfusion. Systemic circulatory support includes intraaortic balloon counterpulsation, cardiopulmonary support, the hemopump, and left heart partial bypass. These support devices, while associated with significant complications, may ultimately improve the safety of coronary angioplasty and allow its application to those who would otherwise not be candidates for revascularization.

Patients with paroxysmal atrial fibrillation (PAF) are prone to recurrence. We compared the efficacy and tolerability of flecainide acetate in the control of PAF by means of conventional treatment with quinidine in 19 patients without structural heart disease. A randomized, placebo-controlled, crossover protocol consisting of 8 weeks of treatment with either agent was used. The recurrence of PAF was documented in a symptom diary and confirmed by event ECG recording. Complete control of symptoms was achieved in 4 of 19 and 2 of 11 of patients with flecainide and quinidine, respectively. Both agents prolonged the time to the first recurrence and significantly reduced the total duration of PAF recurrence by 40% and 47%, respectively (p less than 0.05 compared with placebo). Compared with quinidine, flecainide significantly reduced the frequency of recurrence and the rate of PAF during a recurrent episode. However, treatment with flecainide was associated with a higher incidence of symptomatic sinus pauses and visual disturbances compared with a higher incidence of gastrointestinal side effects with quinidine. During a follow-up period of 32 months, satisfactory control was achieved in 74% of patients with the use of these two antiarrhythmic agents.

Objectives: This study was designed to evaluate the relation between the severity of the residual stenosis of the infarct-related artery and changes in left ventricular volume and function after a first anterior myocardial infarction., Background: Although thrombolytic therapy improves clinical outcome after acute myocardial infarction, the relations between the severity of the residual stenosis of the infarct-related artery and postinfarction left ventricular remodeling and function are unclear., Methods: Fifty-eight patients with a first anterior myocardial infarction and significant disease only in the left anterior descending coronary artery on arteriography performed after 7 to 10 days were evaluated. All patients received thrombolytic therapy. Residual stenosis of the infarct-related artery was measured with quantitative coronary arteriography. Left ventricular volumes and ejection fraction were measured by echocardiography and radionuclide angiography, respectively, 7 to 10 days, 6 months and 1 year after infarction. End-diastolic and end-systolic left ventricular volumes were measured by two-dimensional echocardiography and normalized to body surface area. Patients were classified into three groups according to baseline residual stenosis severity: total occlusion (Group I), minimal lesion diameter less than 1.5 mm (Group II) and minimal diameter greater than or equal to 1.5 mm (Group III)., Results: Group I patients had significantly greater left ventricular end-diastolic and end-systolic volumes at 6 months and 1 year than did the other groups. Group II patients had greater end-diastolic and end-systolic volumes than did Group III patients at 1 year. In addition, Group I patients had a lower ejection fraction at 1 year than that of the other groups. The minimal lesion diameter was significantly correlated with percent change in end-diastolic volume at 1 year., Conclusions: The severity of the baseline residual stenosis of the infarct-related artery is an important predictor of change in left ventricular volumes in the 1st year after infarction. Total occlusion of the infarct-related artery is associated with greater left ventricular dilation and functional impairment.

Electrical alternans and mechanical alternans are intriguing phenomena that have been reported to occur during tachycardias. Their precise pathophysiologic mechanism and in particular their interrelation have not been well defined. This report documents an unusual electromechanical concordance in alternans during sustained supraventricular tachycardia and ventricular tachycardia in two patients, raising interesting possibilities on the underlying mechanism of the concordant phenomena. The findings highlight the principle of excitation--contraction coupling of the heart.

We investigated the potential benefit of a preferential pulmonary vasodilatory effect of nifedipine in 4 patients with Eisenmenger syndrome complicating ventricular septal defect. First-pass radionuclide scan was performed at rest to measure intracardiac shunting before and after nifedipine. Two hours after 20 mg sublingual nifedipine, right-to-left shunt increased from 16.3 +/- 1.4 to 20.4 +/- 1.5% (p less than 0.05), but systemic arterial oxygen saturation (SAO2) remained steady. With 4 weeks of maintenance nifedipine therapy, resting intracardiac shunting and SAO2 were unchanged from baseline. Symptom-limited cycle ergometry was performed before and after maintenance nifedipine with placebo control. Exercise duration was prolonged (8.7 +/- 0.6 vs. 6.8 +/- 0.9 min; p less than 0.02) and SAO2 at each stage of exercise was consistently increased in all patients after nifedipine. Cardiac output and the SAO2 at peak exercise were similar. Thus, chronic nifedipine therapy increases SAO2 on exercise and improves maximal exercise capacity in patients with Eisenmenger syndrome, which is not predicted by study of resting intracardiac shunting after acute therapy.

Background: Studies of normal human coronary dimensions have been performed primarily in postmortem hearts. We evaluated the influence of age, body habitus, and regional myocardial mass on coronary dimensions in living patients with normal coronary vessels., Methods and Results: Arteriographically normal coronary angiograms were analyzed from the following groups of subjects: group 1 (age, 15-34 years) consisted of 30 post-cardiac transplant patients with donor hearts from male subjects aged 15-34 years, group 2 (age, 35-54 years) consisted of 12 post-cardiac transplant patients with donor hearts from male subjects aged 35-54 years and 26 male subjects investigated for atypical chest pain, and group 3 (age, 55-74 years) consisted of 26 male subjects investigated for atypical chest pain. All angiograms were performed after sublingual nitroglycerin. Measurements of the dimensions of the left main, proximal left anterior descending, proximal left circumflex, and proximal right coronary arteries were made using a computer-assisted edge-detection algorithm. The regional myocardial mass supplied by each vessel was derived from echocardiographically derived total left ventricular mass and a semiquantitative angiographic territory scoring system based primarily on the number and length of its terminal nutrient branches., Conclusions: Linear regression analysis showed that coronary vessel cross-sectional area and total coronary cross-sectional area increase with regional myocardial mass and decrease linearly with age. Multivariate regression analysis revealed that regional myocardial mass and age were independent predictors of cross-sectional area for each vessel and for the total coronary cross-sectional area. We speculate that age-related decline in physical activity, in part, may be responsible.

A computerized system designed to optimize the quantitation of coronary vessels on 35 mm cineangiograms is described and validated. Because the system has two cine film digitizers, it processes paired coronary arteriograms for the evaluation of serial changes in coronary arteries. A database system was specifically designed for the storage of coronary artery quantitation data which resides on a file server in a local area network and may be accessed by multiple workstations. In radiographic phantom studies of nine contrast-filled lucite cylinders of known size, the overall accuracy and precision for the measured diameters were 0.069 mm and 0.066 mm respectively. Measurements of minimum diameter and percent diameter stenosis of 21 coronary lesions selected from 17 routine cineangiograms showed high degree of intraobserver and interobserver reproducibility.

Background: Platelet deposition at the site of injury caused by balloon angioplasty is associated with acute closure and restenosis., Methods and Results: In a new ex vivo whole artery angioplasty model, we examined the roles of thrombin inhibition with D-Phe-Pro-ArgCH2Cl (PPACK) and inhibition of the platelet membrane fibrinogen receptor glycoprotein IIb/IIIa (GPIIb/IIIa) with monoclonal antibody 7E3 on platelet deposition at the site of balloon injury. Fresh rabbit aortas were mounted in a perfusion chamber. One half of the mounted arterial segment was dilated with a standard angioplasty balloon catheter and the uninjured half served as the control segment. The vessels were perfused with human blood at physiological pressure and shear rates of 180-250 second-1 for 30 minutes. Platelet deposition was measured using 111In-labeled platelets and scanning electron microscopy. With heparin (2 units/ml) anticoagulation, 8.2 +/- 2.2 x 10(6) platelets/cm2 were deposited at the site of balloon injury compared with 0.7 +/- 0.2 x 10(6) platelets/cm2 on uninjured segments (p less than 0.02, n = 7). PPACK was tested at a concentration (10 microM) that totally inhibited platelet aggregation in response to thrombin. 7E3 was tested at a concentration (10 micrograms/ml) that totally inhibited platelet aggregation. Platelet deposition at the site of balloon injury was reduced 47% by PPACK and 70% by 7E3 compared with heparin., Conclusions: At shear rates seen in nonstenotic coronary arteries, PPACK and 7E3 are more effective than heparin in reducing platelet deposition at the site of balloon injury. The significant inhibition of platelet deposition by PPACK demonstrates the importance of heparin-resistant thrombin in platelet thrombus formation. The 7E3 results suggest that approximately 70% of platelet deposition at the site of balloon injury is GPIIb/IIIa dependent and that the remaining 30% results from non-GPIIb/IIIa-mediated platelet-subendothelial adhesion. Finally, the ex vivo whole artery system is a useful model for studying platelet-vessel wall interactions under physiologically defined parameters.

Gangrene of the left upper limb was found to complicate severe mitral stenosis presenting with heart failure in a sixty-eight-year-old woman with a documented left atrial thrombus. Arterial obstruction as the cause of gangrene was excluded by Doppler-assisted assessment of the peripheral pulses. Venous gangrene can complicate severe mitral stenosis and must be distinguished from arterial embolization, in which urgent surgical treatment is imperative.

This study evaluates the changes in left ventricular (LV) diastolic filling after percutaneous transluminal coronary angioplasty and the relation of such changes to quantitative angiographic measurements of the severity of coronary narrowings. Pulsed Doppler echocardiographic measurements were performed in 40 patients with single left anterior descending artery narrowing before, and 10 and 30 days after angioplasty. Minimal luminal diameter and percent diameter stenosis of coronary lesions were measured by computer-assisted quantitation. The ratio of early to late diastolic flow velocities (E/A ratio), time velocity integral of early diastolic filling period (Ei) and the ratio of early and late diastolic filling periods (Ei/Ai ratio) increased gradually after angioplasty. Minimal luminal diameter correlated significantly with the percent changes in E/A ratio (r = 0.59 at 10 days, r = 0.57 at 30 days), Ei (r = 0.53 at 10 days, r = 0.55 at 30 days) and Ei/Ai ratio (r = 0.41 at 10 days, r = 0.49 at 30 days). Percent diameter stenosis showed overall weaker correlations than minimal diameter with the percent changes in E/A ratio (r = 0.39 at 10 days, r = 0.32 at 30 days) and Ei (r = 0.38 at 10 days, r = 0.31 at 30 days). Thus, LV diastolic filling improves serially after coronary angioplasty in patients with 1-vessel disease. The magnitude of improvement in diastolic filling correlates better with minimal luminal diameter than percent diameter stenosis. Therefore, minimal luminal diameter is a better predictor of changes in Doppler transmitral flow parameters after angioplasty than percent diameter stenosis.

A questionnaire study was carried out among cardiologists, internists, general practitioners, and final year medical students in Hong Kong concerning cardiac pacemaking. The response rate was 11.2%. Salient results include the misconception on the part of 40% and 12% of physicians, that general anesthesia and thoracotomy respectively, are commonly required for permanent pacing and that the procedure is associated with significant mortality (14.2% of physicians). Most would offer permanent pacing to patients with symptomatic complete atrioventricular block, but advanced age appeared to be considered as a barrier to permanent pacemaking. There was confusion about the need to pace asymptomatic sick sinus syndrome and bundle branch conduction diseases. Oral isoprenaline was still used to treat bradycardia by 16.6% of physicians. A similar deficiency in knowledge was found among the students. It is suggested that misunderstanding of cardiac pacing is common and may be a reflection of the lack of emphasis in undergraduate teaching. This deficiency may have prevented some patients from receiving the benefits of permanent pacing.

A patient with an aortic root abscess complicating Mycobacterium fortuitum prosthetic endocarditis is described. The correct diagnosis had been made preoperatively by echocardiography and was confirmed subsequently at surgery.

The relative hemodynamic profile between dual chamber pacing (DDD) and activity sensing rate responsive pacing (VVIR) was compared in ten patients with dual chamber rate responsive pacemakers (Synergist II). With a double blind, randomized exercise protocol, DDDR pacemakers were programmed into VVI, VVIR, and DDD (AV interval 150 msec) modes and in seven patients the test in the DDD mode was repeated with the AV interval programmed at 75 msec. A treadmill exercise test of 6-minutes duration (2 stages, Stage I at 2 mph, 0% gradient and Stage II at 2 mph, 15% gradient) was performed at each of the programmed settings, with a rest period of 30 minutes in between tests. Cardiac output was assessed using continuous-wave Doppler sampling ascending aortic flow and expressed as a percentage of the value achieved during VVI pacing. During exercise, pacing rate between DDD and VVIR pacing was similar but was higher with DDD at the first minute of recovery (91 +/- 4 vs 81 +/- 3 beats/min, respectively). Cardiac output was significantly higher at rest, during low level exercise, and recovery with DDD pacing compared with VVIR pacing (resting: 21 +/- 14 vs -2 +/- 7%; Stage I: 36 +/- 6 vs 16 +/- 7%; Stage II: 25 +/- 15 vs 10 +/- 8%; recovery: 26 +/- 12 vs 4 +/- 9%; P less than 0.05 in all cases). Systolic blood pressure was significantly higher during low level of exercise in the DDD mode. Shortening of the AV interval to 75 msec did not significantly affect cardiac output during exercise, but cardiac output after exercise was reduced (2 +/- 6 vs 23 +/- 6% at an AV interval of 150 msec, P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Beta-adrenergic blocking agents are useful in controlling excessive ventricular rate in chronic atrial fibrillation (AF) but often reduce exercise capacity. To investigate the advantage of labetalol--a unique beta blocker with alpha-blocking property--in chronic AF, 10 patients without underlying structural heart disease were studied with treadmill test, 12-minute walk and 24-hour ambulatory electrocardiographic monitoring. Patients were randomized and crossed over to receive 4 phases of treatment (placebo, digoxin, digoxin with half-dose labetalol, and full-dose labetalol). Exercise durations were 14.1 +/- 1.5, 14.2 +/- 1.5, 16.1 +/- 1.1 and 15.6 +/- 1.1 minutes, respectively, indicating that labetalol did not reduce exercise tolerance. Although digoxin had no advantage over placebo in controlling maximal heart rate (177 +/- 2 vs 175 +/- 3 beats/min), labetalol, both as monotherapy or as an adjunct to digoxin, was advantageous (156 +/- 4 vs 177 +/- 2 beats/min, p less than 0.01, and 154 +/- 4 vs 177 +/- 2 beats/min, p less than 0.01, respectively). The rate-pressure product was consistently lowered by labetalol at rest and during exercise. At peak exercise, the addition of labetalol to digoxin reduced the maximal rate-pressure product achieved from 30,900 +/- 1300 to 24,100 +/- 2,000 mm Hg/min (p less than 0.01) and the maximal rate-pressure product was lowest with full-dose labetalol (22,300 +/- 1,600 mm Hg/min). During submaximal exercise on treadmill or during the 12-minute walk, the combination of labetalol and digoxin produced the best heart rate control, whereas labetalol monotherapy was comparable to digoxin therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Measurement of coronary dimension requires an accurate and reproducible dimensional reference. Angiographic catheters are frequently used for this purpose. We measured the angiographic diameters of a broad range of diagnostic and angioplasty guiding catheters by using two commonly used edge-detection algorithms. Angiographic diameters are significantly less than true catheter outer diameter. Therefore the use of contrast-filled catheters as a dimensional reference may lead to considerable error in vessel measurement with overestimation of absolute dimension. Tables of reference values for multiple catheter as calibration standard, tested under a variety of angiographic conditions. The metallic-tipped marker was found to have a better degree of reproducibility than catheters. These findings have implications for studies employing serial measurements of coronary artery dimension and for the clinical practice of estimating vessel diameter for choice of balloon size during angioplasty.

The influence of heart rate changes on the recovery of cardiac hemodynamics and lactate clearance after exercise was studied in nine patients with complete atrioventricular (AV) block treated with programmable pacemakers. A preliminary treadmill exercise test in which the pacing rate was externally increased stepwise from 70 to 130 bpm was performed to determine the maximum exercise duration. Two exercise tests involving an equal amount of exercise load were performed, the pacing rate was either programmed to the basic rate (abrupt decay) or gradually (modulated decay) immediately after exercise termination. Compared with abrupt decay, modulated decay resulted in a higher mean arterial pressure (100 +/- 4 mmHg vs 91 +/- 5 mmHg, P less than 0.05) and diastolic pressure (76 +/- 4 mmHg vs 59 +/- 4 mmHg, P less than 0.001) immediately on exercise termination. Immediately after exercise and during modulated decay, cardiac output (represented by Doppler derived minute distance) declined gradually and was determined mainly by a higher pacing rate without significant changes in stroke volume. On the other hand, minute distance fell abruptly during abrupt decay (996 +/- 107 m at peak exercise and 561 +/- 88 m immediately after a rate change at exercise termination, P less than 0.01) with a corresponding abrupt increase in systemic vascular resistance. This was later compensated by a gradual increase in stroke volume during the recovery period. The cumulative cardiac output between the two rate changes equalized at the 4th minute of recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Purpose: Although the antiphospholipid antibodies are well recognized to be associated with thrombosis, recurrent abortion, and thrombocytopenia in patients with systemic lupus erythematosus (SLE), their relationship with cardiac disease is less clear. The purpose of this study was to evaluate the association between anti-phospholipid antibodies and cardiac abnormalities in patients with SLE., Patients and Methods: A total of 75 consecutive SLE patients and 60 healthy sex- and age-matched control subjects were evaluated in a case-control study. All participants underwent M-mode, two-dimensional, and Doppler echocardiography. Antiphospholipid antibodies levels were assayed in each patient. The prevalence of antiphospholipid antibodies in patients with and without echocardiographic abnormalities was compared., Results: Compared with the control group, SLE patients had significantly more pericardial abnormalities, left ventricular hypertrophy, left atrial enlargement, left ventricular dysfunction and verrucous valvular thickening, global valvular thickening with dysfunction, and mitral and aortic regurgitation. Among these abnormalities, antiphospholipid antibodies were significantly associated with isolated left ventricular (global or segmental) dysfunction (four of five positive; p less than 0.05), verrucous valvular (mitral or aortic) thickening (seven of nine positive; p less than 0.005), global valvular (mitral or aortic) thickening and dysfunction (five of six positive; p less than 0.02), as well as mitral regurgitation (16 of 19 positive; p less than 0.001) and aortic regurgitation (five of six positive; p less than 0.02)., Conclusion: Valvular lesions and myocardial dysfunction are associated with elevated antiphospholipid antibodies. This study has important implications for the pathogenic role of anti-phospholipid antibodies in relation to these cardiac abnormalities.

The effect of an abrupt reduction in atrial pressures on atrial natriuretic peptide (ANP) secretion was studied in four patients with complete atrioventricular block with a dual-chamber pacemaker when the pacing mode was changed from the VVI to the DVI mode at an equal rate of 70/min. Simultaneous continuous hemodynamic monitoring was performed using a balloon-tipped thermodilution catheter. With DVI pacing, there was an immediate decrease of right atrial pressure from 4.5 +/- 0.9 to 1.8 +/- 1.1 mm Hg, and a reduction of pulmonary arterial wedge pressure from 7 +/- 0.8 to 4.5 +/- 0.9 mm Hg, together with a rise in cardiac output from 3.1 +/- 0.2 to 3.7 +/- 0.2 L/min. However, despite a constant hemodynamic status after dual-chamber pacing, the arterial ANP level steadily decreased from 151 +/- 26 pg/ml to a steady low level of 78 +/- 15 pg/ml after 20 minutes of dual-chamber pacing (percentage reduction- 48 +/- 8%, p less than 0.05). This persisted until the end of the study at 60 minutes. The time-dependent decay in ANP secretion after an abrupt and constant change in hemodynamic status should be considered when interpreting ANP levels.

Pericardial nocardiosis is extremely rare, but may affect especially immunocompromised hosts. We describe the first reported case of purulent pericarditis with cardiac tamponade as the initial presentation of systemic nocardiosis in a patient with mixed connective tissue disease. Our case emphasizes the importance of identifying infectious causes of pericarditis in patients with connective tissue diseases. Longterm survival was achieved with a combined medical and surgical approach.

The effects of short- and long-term calcium replacement on myocardial function in six asymptomatic patients (age 48 +/- 3, mean +/- SEM) with hypocalcemia complicating surgical hypoparathyroidism were studied. Cardiac output was determined by ascending aortic continuous wave Doppler assessment and was measured as minute distance. During intravenous calcium replacement at rest, ascending aortic minute distance increased from 6.75 +/- 1.10 to 9.17 +/- 1.29 m as the calcium level rose from 1.76 +/- 0.08 to 2.06 +/- 0.19 mmol/L without changes in heart rate and blood pressure (p less than 0.01). The peak velocity and acceleration of blood flow derived from Doppler measurement showed a similar rise during calcium infusion. Symptom-limited cycle ergometry was performed before and 3 months after normalization of calcium by long-term oral therapy. Although the resting cardiac output was unchanged, the maximum cardiac output at peak exercise also increased from a minute distance of 11.58 +/- 1.84 to 15.37 +/- 2.28 m (p less than 0.05), together with an increase of maximum heart rate from 136 to 149 beats/min (p less than 0.05). Exercise duration was also prolonged from 11.9 +/- 2.9 to 13.0 +/- 2.8 minutes. Thus hypocalcemia impairs cardiac performance, but this impairment is reversible with calcium replacement.

We report a case of aneurysmal coronary sinus complicating severe valvular disease with severe tricuspid regurgitation. Injection in the left superior vena cava outlines the aneurysmal coronary sinus with stasis of the contrast. As this anomaly carries special surgical implication in patients requiring open heart surgery, a correct preoperative diagnosis is mandatory.

Subclinical myocardial involvement frequently occurs in patients with systemic lupus erythematosus (SLE). In this study, left ventricular diastolic function was assessed in 58 patients (54 female and 4 male; mean age 32 +/- 11 years) and in 40 sex-matched and age-matched healthy control subjects (37 female and 3 male; mean age 33 +/- 9 years) by means of pulsed Doppler echocardiography. All subjects had no clinical evidence of overt myocardial disease or abnormal left ventricular systolic function. Compared with the control group, patients with SLE had significantly prolonged isovolumic relaxation time (62 +/- 12 vs 80 +/- 14 msec; p less than 0.01), reduced peak early diastolic flow velocity (peak E) (82 +/- 18 vs 76 +/- 16 cm/sec; p less than 0.05), increased peak late diastolic flow velocity (peak A) (45 +/- 7 vs 53 +/- 8 cm/sec; p less than 0.01), reduced E/A ratio (1.81 +/- 0.32 vs 1.46 +/- 0.29; p less than 0.001), and lower deceleration rate of early diastolic flow velocity (EF slope) (489 +/- 151 vs 361 +/- 185 cm/sec2; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

A prospective M-mode, cross-sectional and Doppler echocardiographic study was performed on 75 patients with systemic lupus erythematosus and 60 sex- and age-matched control subjects. Compared with the control group, patients with lupus had an increased prevalence of echocardiographic abnormalities. These included pericardial effusion and/or thickening (37%), left ventricular hypertrophy (12%), global left ventricular hypokinesis (5%), segmental abnormalities of left ventricular wall motion (4%), right ventricular enlargement (4%), focal verrucous valvar thickening (12%), gross valvar thickening and dysfunction (8%), mitral regurgitation (25%) and aortic regurgitation (8%). Two patients with gross mitral valvar thickening and dysfunction subsequently underwent valvar replacement. Correlation between echocardiographic abnormalities and clinical parameters showed that pericardial effusion was significantly associated with pericardial pain (P less than 0.05) and active disease (P less than 0.001), and left ventricular hypertrophy with systemic hypertension (P less than 0.05). Thus, there was a high prevalence of cardiac abnormalities, especially pericardial and valvar lesions, in patients with systemic lupus erythematosus. Echocardiography is invaluable in identifying these abnormalities and should be used routinely for cardiac evaluation of these patients.

Catheter-associated candidemia is a common problem in immunocompromised patients. A leukemic patient had Candida right ventricular mural endocarditis complicating an indwelling right atrial catheter. To our knowledge, this is the first reported case of Candida right ventricular mural vegetation visualized by two-dimensional echocardiography.

In 15 patients with atrial fibrillation (AF), a single right ventricular extrastimulus (intercalated pacing) was delivered after every sensed conducted beat resulting in a reduction in rate. This method was used in 10 patients with lone AF and the average success rate of inducing coupling was 86 +/- 14% (range 64 to 100), using a mean coupling interval of 232 +/- 28 ms (range 175 to 290). During intercalated pacing, the pulse rate of AF was reduced (from 137 +/- 26 to 75 +/- 14 beats/min, p less than 0.001). Intercalated pacing resulted in enhancement of mean stroke volume (28 +/- 6 vs 44 +/- 10 ml in AF, p less than 0.0001), pulse pressure and the pulse-to-pulse regularity. Both the systolic and diastolic arterial pressures were regularized. The reduction in pulse rate during intercalated pacing was determined by the coupling interval, and the induction of concealed ventriculoatrial conduction (82 +/- 44 ms). Myocardial lactate extraction was similar during AF and short-term intercalated pacing (28 +/- 10 vs 25 +/- 9%, difference not significant). In 5 patients with severe mitral stenosis in AF, intercalated pacing resulted in an improvement in the cardiac output (3.1 +/- 0.2 vs 3.4 +/- 0.2 liters/min, p less than 0.04), a reduction in the gradient across the mitral valve (16 +/- 8 vs 10 +/- 5 mm Hg, p less than 0.02), and a reduction in pulmonary arterial and wedge pressures. This new pacing method thus achieved rapid temporary control of rate, regularity and cardiac hemodynamics during AF, which were more prominent in patients with mitral stenosis and restricted left ventricular filling.

A patient is described with quinidine-induced acute lymphadenopathy syndrome proven by rechallenge of the drug. Serum markers for systemic lupus were negative.

To evaluate cardiac involvement in mixed connective tissue disease (MCTD), M-mode, 2-dimensional and pulsed Doppler echocardiography were performed in 17 patients with MCTD. Pericardial abnormalities were present in 4 patients (24%), including small pericardial effusion (less than 1 cm) in 2 patients and pericardial thickening in 2 patients. Verrucous thickening of the mitral valve was detected in 2 patients (12%) by 2-dimensional echocardiography. Pulsed Doppler echocardiography revealed the presence of mild mitral regurgitation in one of them. To our knowledge, such mitral valve abnormalities have not been reported. Future larger studies are needed in order to evaluate the incidence and natural evolution of these mitral valvular abnormalities.

Labetalol, a combined alpha- and beta-blocking agent, was administered to 12 patients (mean age 55 years) with idiopathic dilated cardiomyopathy to examine its effects on symptomatology and exercise performance. Studies were performed before treatment, after 8 weeks of placebo, and after 8 weeks of labetalol therapy in a randomized, crossover, double-blind design. The mean (+/- SEM) dose of labetalol for the group was 275 +/- 29 mg. Compared to treatment with placebo, the maximum duration of symptom-limited exercise was significantly prolonged with labetalol (580 +/- 72 seconds to 683 +/- 71 seconds; p less than 0.005). Both the resting and peak exercise heart rate and systolic blood pressure were significantly reduced. Ascending aortic blood flow velocity was also measured by continuous-wave Doppler technique during exercise. Compared to placebo, treatment with labetalol conferred no significant change in cardiac output at rest but significantly improved cardiac output at maximum exercise (14 +/- 3%; p less than 0.001). Doppler-derived peak aortic flow velocity, acceleration, and flow velocity integral were also significantly improved at maximum exercise. Systemic vascular resistance, as derived from mean blood pressure/cardiac output, was reduced by 12 +/- 3% and 16 +/- 3% at rest and at maximum exercise, respectively. New York Heart Association functional class was improved (3.2 +/- 0.2 to 2.2 +/- 0.3; p less than 0.005). No major side effects from labetalol were encountered. Thus labetalol improves symptomatology, exercise capacity, and exercise hemodynamics and reduces systemic vascular resistance in patients with idiopathic dilated cardiomyopathy.

The haemodynamics and myocardial lactate consumption during induced atrial fibrillation (AF) were studied in 10 patients with paroxysmal AF. Their mean age (+/- SD) was 61 +/- 5 years and none had clinical evidence of ischaemic or rheumatic heart disease. Compared with sinus rhythm, the onset of AF was associated with a reduction in systolic blood pressure (152 +/- 13 mmHg) in AF vs 169 +/- 23 mmHg in sinus rhythm, P less than 0.01). There was no consistent change in cardiac output at the onset of AF compared with sinus rhythm, but the cardiac output was lower compared with regular atrial pacing at rates similar to those of induced AF (3.85 +/- 0.76 vs 4.38 +/- 0.89 l min-1, P less than 0.02). Compared with sinus rhythm or rate-matched atrial pacing, AF was associated with an elevated pulmonary arterial pressure (24.2 +/- 5.6 mmHg in AF vs 17.9 +/- 14.4 mmHg in sinus rhythm, P less than 0.01) and pulmonary arterial wedge pressure (18.6 +/- 5.6 vs 9.7 +/- 3.9 mmHg, P less than 0.01). The haemodynamic changes during AF were similar to those seen during regular ventricular pacing at an equivalent rate, although the latter was associated with a lower systolic blood pressure (152 +/- 13 mmHg in AF vs 136 +/- 25 mmHg in ventricular pacing, P less than 0.05) and higher right atrial pressure (8.2 +/- 4.4 vs 11.5 +/- 7.5 mmHg respectively, P less than 0.05), presumably due to the deleterious effects of cannon 'a' waves.(ABSTRACT TRUNCATED AT 250 WORDS)