Noninvasive estimation of coronary flow reserve by transesophageal Doppler measurement of coronary sinus flow.
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Biomedical subjects
Publications and source records attributed to G Kreiner.
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To study the age-related differences in Wolff-Parkinson-White syndrome an elderly group of 20 patients aged 40-65 years was compared to a younger group of 26 patients aged 18-39 years with respect to clinical profile and electrophysiological characteristics. The two groups were comparable in terms of the mechanism of reentry tachycardia, accessory pathway location, the number of patients reporting syncopal episodes, and the incidence of inducible and/or documented atrial flutter/fibrillation while only elderly patients had also atrial tachycardias. The elderly group was characterized by a higher incidence of associated organic heart disease and a significantly higher percentage of resuscitation from circulatory arrest. Cardiocirculatory arrest due to arrhythmias was the event leading to transferral to our hospital in 30% of elderly patients compared with 7.7% in the younger group. Analogous results were obtained when stratified according to the age at manifestation of tachyarrhythmias (< 30, > or = 30 years), a history of cardiopulmonary resuscitation being the only significant difference between the two groups. There was no difference in any electrophysiologic parameter between the two age groups or with respect to the age at manifestation of arrhythmias. It is concluded that elderly patients with the Wolf-Parkinson-White syndrome should be managed as aggressively as their younger counterparts. In particular, manifestation of arrhythmias due to Wolff-Parkinson-White syndrome beyond age 30 should not be regarded as a more benign variation of the syndrome. Explanations for the more frequent history of resuscitation in the elderly include the presence of organic heart disease with impairment of left or right ventricular function and differences in the management of these patients.
The purpose of the present study was to evaluate the specific role of hemorheologic and hemodynamic parameters for spontaneous echo contrast and thrombus formation in vivo. We therefore investigated the association between the presence of left atrial spontaneous echo contrast and thrombus formation by transesophageal echocardiography and multiple clinical, hemodynamic, and hemorheologic parameters in 70 patients with idiopathic dilated cardiomyopathy. Transesophageal echocardiography showed left atrial spontaneous echo contrast and left atrial thrombi in 33% and 19% of patients, respectively. Patients with left atrial spontaneous echo contrast had a lower cardiac index (2.1 +/- 0.9 versus 2.6 +/- 0.9 L/min/m2; p < 0.02), a lower left atrial (21 +/- 8 versus 38 +/- 10 cm/sec; p < 0.001) and left atrial appendage flow velocity (17 +/- 14 versus 39 +/- 13 cm/sec; p < 0.001), a larger left atrial diameter (53 +/- 6 versus 46 +/- 10 mm; p < 0.002), and more often presented with atrial fibrillation (62% versus 32%; p < 0.02). Plasma fibrinogen concentration (4.0 +/- 1.1 versus 3.5 +/- 0.7 gm/L; p < 0.02) and plasma viscosity (1.83 +/- 0.10 versus 1.76 +/- 0.15 mPa.sec; p < 0.05) were higher in patients with spontaneous echo contrast. Multivariate analysis revealed an association between the presence of spontaneous echo contrast and left atrial flow velocity p < 0.0001) and plasma viscosity (p < 0.01). In patients with left atrial (appendage) thrombus or a history of embolism, left atrial appendage flow velocity was lower (15.0 +/- 8.2 versus 29.6 +/- 14.5 cm/sec; p < 0.005) and spontaneous echo contrast was more frequently observed (52% versus 23%; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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The impact of a right bundle branch block (RBBB), inadvertently created prior to complete ablation of the atrioventricular (AV) junction, on the intrinsic subsidiary pacemaker function was investigated. In 31 patients suffering from intractable supraventricular tachyarrhythmia, catheter ablation of the AV junction was performed using direct current (n = 13) or radiofrequency (n = 18) energy. In 16/31 patients a RBBB was created prior to complete AV ablation. Subsidiary pacemaker function was evaluated after a mean period of 5 months. Following 5 min of ventricular pacing (70 beats.min-1) escape interval and spontaneous heart rate were measured. In patients with a RBBB there was a trend towards a longer escape interval (2979 +/- 2559 vs 1867 +/- 1254 ms, P = ns) and a significantly lower intrinsic heart rate (38 +/- 14 vs 47 +/- 8 beats.min-1, P < 0.05). Pacemaker dependency was only observed among patients with a RBBB (4/16 vs 0/15, P < 0.05). HV intervals were shorter in those energy discharges resulting in a RBBB as compared to those inducing a complete heart block (52 +/- 8 vs 66 +/- 6 ms, P < 0.05). Creation of a RBBB prior to complete ablation of the AV junction results in impaired intrinsic subsidiary pacemaker function; the most proximal catheter position should be carefully sought to minimize the risk of pacemaker dependency.
Severe heart failure developed in a 49-year-old patient 18 months after orthotopic cardiac transplantation. Acute rejection as well as other overt causes of graft failure were excluded. Haemodynamic measurements suggested severe diastolic myocardial dysfunction. Since no other causes of diastolic heart failure were identified, a potential side effect from cyclosporine was considered. Cyclosporine was therefore withdrawn and immunosuppressive treatment was switched to conventional therapy consisting of azathioprine and prednisolone. Withdrawal of cyclosporine was followed by an impressive clinical improvement and by complete haemodynamic normalization. Therefore, in cases of otherwise unexplained graft failure, a potentially reversible side effect from cyclosporine should be taken into consideration.
In a patient with a left sided accessory pathway (AP) three different types of orthodromic circus movement tachycardia were observed: (1) narrow QRS complex tachycardia with a stable cycle length (CL); (2) wide QRS complex tachycardia with a functional bundle branch block ipsilateral to the AP, which, paradoxically, had a shorter CL. The decrease in CL was due to a decrease of the AH interval; and (3) narrow QRS complex tachycardia with alternating CL, due to alternations of the AH interval. These phenomena were attributed to a concomitant dual atrioventricular (AV) node, which was eventually proven after successful catheter ablation of the AP.
The chronotropic response during graded, symptom limited exercise was investigated in 32 cardiac transplant recipients a mean of 49 +/- 18 days after transplantation. All patients had systematic evaluation of postoperative donor sinus node (SN) function and the cardioacceleratory response was compared according to the SN function. Twenty-one patients had normal postoperative SN studies (corrected SN recovery time < 520 msec, group I) while the SN function was impaired postoperatively in the remainder (n = 11, group II; corrected SN recovery time 4,149 +/- 6,283 msec in 5 patients, junctional escape rhythm in 6 patients). All patients had regained sinus rhythm at time of the exercise test. Patients in group II had lower basal sinus rates at the beginning of exercise (91.5 +/- 11 vs 101.4 +/- 7 beats/min, P < 0.02). This lower chronotropy was maintained over every incremental step (F rate between groups = 30, P = 0.0001, F rate vs workload = 15, P = 0.0001 by two-way ANOVA) and resulted in a significantly lower heart rate at individual peak exercise (108.3 +/- 20 vs 124.2 +/- 13 beats/min, P < 0.02). A total of 14/16 patients in group I but only 2/16 patients in group II accomplished a peak heart rate > or = 120 beats/min (P = 0.009). The workload achieved did not differ between the groups (107 +/- 29 vs 102 +/- 32 watts, P > 0.5). These data show a lower SN chronotropy during rest and at peak exercise in cardiac transplant recipients with postoperative SN deficiency and apparent normalization of SN function.
Postoperative atrioventricular nodal (AVN) function was compared in 55 patients with normal and 50 patients with impaired sinus node (SN) function after cardiac transplantation (corrected SN recovery time > 520 msec or sinus arrest +/- escape rhythm). Fifty-two patients had fixed atrial pacing at cycle lengths between 600 and 430 msec, and 53 patients at cycle lengths from 600 to 300 msec between postoperative weeks 1 to 3. Relative (stimulus-R interval; AVNRRP) and effective AVN refractory period (AVNERP) were determined in 53 patients at a cycle length of 500 msec. Only one of 105 recipients had high degree AVN conduction disturbance characterized by a Wenckebach phenomenon at cycle length < 630 msec in the first postoperative week. Three patients with normal and two patients with impaired SN function had Wenckebach cycle lengths > 430 msec while the Wenckebach cycle lengths were < or = 430 msec in the remainder (p = NS). Resting PQ interval (146 +/- 18 vs 162 +/- 32; p = 0.09), Wenckebach cycle length (350 +/- 53 vs 362 +/- 50 msec), AVNRRP (356 +/- 38 vs 367 +/- 37 msec), and AVNERP (217 +/- 48 vs 244 +/- 49 msec) did not differ significantly between patients with normal and impaired SN function. AVN conduction did not deteriorate during 318 +/- 130 days of follow-up (PQ at follow-up 154 +/- 17 and 158 +/- 22 msec, patients with normal and impaired SN function, respectively). One DDD pacemaker was placed for AVN conduction disturbance while 22 pacemakers were implanted for SN deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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Incessant supraventricular tachyarrhythmia may lead to a reversible impairment of left ventricular (LV) function. This issue was investigated in 10 patients (aged 64 +/- 13 years) who underwent radiofrequency His bundle ablation for control of drug refractory, chronic atrial fibrillation (n = 9) and recurrent atrial flutter (n = 1). LV function was assessed by 2-dimensional guided M-mode echocardiography within 24 hours (baseline) and 49 +/- 18 days (follow-up) after successful ablation, both during VVI pacing at 70 beats/min. Fractional shortening increased from 28 +/- 9% at baseline to 35 +/- 8% at follow-up (p = 0.006). This increase in fractional shortening was due to a significant reduction of end-systolic diameter from 41 +/- 10 to 36 +/- 10 mm (p = 0.02), whereas there was no appreciable change in end-diastolic diameter (56 +/- 7 to 55 +/- 10 mm; p = 0.5). These changes were substantially greater in patients with baseline impairment of LV function (fractional shortening less than 27%). Fractional shortening increased by 12% (p = 0.14) in patients with normal LV function (n = 5) and by 44% (p = 0.02) in those with impaired LV function at baseline (n = 5). The greater increase in fractional shortening in patients with preexisting LV impairment was due to a more pronounced decline in end-systolic dimensions (-11.9%; p = 0.08) compared with that of patients with normal LV function at baseline (-9.21%; p = 0.2). End-diastolic diameter showed no significant change in either group (-3.53% [p = 0.8] and -0.58% [p = 0.4]).(ABSTRACT TRUNCATED AT 250 WORDS)
Nine adult patients with Ki-1-positive large-cell anaplastic lymphoma were treated with MACOP-B. Two suffered from relapsed disease and had previously received chemotherapy; a third patient had received a single dose of 100 mg/m2 cisplatin before initiation of MACOP-B. The stage of lymphoma was determined according to the Ann Arbor Conference criteria and was II in one, III in two and IV in six patients. All patients had constitutional symptoms. Five patients had achieved complete remission 4 weeks after termination of the protocol and there were two partial remissions. One patient died of massive pulmonary embolism during the 4th week of treatment; another patient, who had received MACOP-B as salvage therapy, died of progressive lymphoma 1 month after completion of the regimen. Maximal observed toxicities according to WHO were mucositis grade 3 (n = 3) and there were three cases with thromboembolic complications, including a fatal pulmonary embolism in a young patient. However, MACOP-B appears an effective, fairly well-tolerated and feasible therapy for patients with Ki-1-positive large-cell anaplastic lymphoma.
A young male patient progressed rapidly from localized abdominal lymph node enlargement to overt acute lymphoblastic leukemia. Despite aggressive treatment, he died of progressive CNS leukemia 5 months after initial presentation. At diagnosis, karyotypic analysis of an abdominal lymph node revealed the coexistence of t(14;18) (q32;q21), specific for follicular lymphoma, and t(8;22) (q24;q11), a variant Burkitt translocation. Such cases might be considered as a model for a general mechanism of tumor progression with cascade-like involvement of oncogenes.
The acute haemodynamic effects of seven different drugs were serially evaluated in eight patients suffering from pulmonary hypertension of unknown cause. The following drugs were tested in randomized order: nifedipine, amrinone, isoproterenol, captopril, prostacyclin, dihydralazine and nitroglycerin. Only a reduction in pulmonary vascular resistance (PVR) of more than 30% of baseline was considered a satisfactory response. Overall, the decrease in PVR ranged from 9 +/- 12% (nitroglycerin) to 38 +/- 23% (prostacyclin). However, marked inter- and intra-individual variability in the efficacy of all drugs was observed, making cross reactivity totally unpredictable. The number of responders for each drug varied between five (prostacyclin) and zero (dihydralazine, nitroglycerin). Conversely, a maximum of three drugs was capable of eliciting a response in an individual patient, with only two out of eight patients being total non-responders. A reduction in PVR of more than 30% (n = 16) was associated with a significant decrease in mean pulmonary artery pressure (49.1 +/- 8.2 versus 39.4 +/- 6.4 mmHg) and a significant increase in cardiac index (2.5 +/- 0.6 versus 3.4 +/- 0.8l.min-1.m-2). Overall, none of the drugs tested proved to be clearly superior. However, because of marked inter- and intra-individual variability, the therapeutic approach must be based on trial and error and the evaluation of all drugs is indicated if one fails.
Fifteen cardiac transplant recipients requiring permanent pacing (AAI, n = 9; VVI, n = 6; rate responsive devices, n = 11) for postoperative sinus node (SN) insufficiency underwent evaluation of long-term SN function 240 to 1,461 days after transplantation. The intrinsic rhythm at the time of discharge was sinus in 7 patients; junctional escape in 6 patients; and pacemaker dependent in 2 patients. At follow-up, 5 patients had regained regular sinus rhythm, accounting for a total of 11 patients in sinus rhythm while 4 patients were in junctional bradycardia. The SN recovery time as determined by the permanent pacemaker was normal (< 1,500 msec) in only 1/8 patients in whom it was determined, although 4 of these 8 patients were temporarily overriding the pacemaker during ambulatory monitoring. Patients with pathological SN recovery times included 3 patients with late return of sinus rhythm and 4 patients who had recovered normal sinus rhythm before their discharge from the hospital. Three patients developed late symptoms despite apparent early normalization and underwent delayed pacemaker implantations on postoperative days 35, 52, and 225, respectively. We conclude that, in patients requiring pacemaker implantation after cardiac transplantation, normalization of SN function cannot be inferred from just return of sinus rhythm, regardless of whether it occurs early or late. These findings may have implications when a pacemaker exchange or explantation is being considered.
Time and frequency domain parameters of heart rate variability (HRV) were determined in patients with severe endstage heart failure awaiting cardiac transplantation (HTX). These parameters were then correlated with mortality to investigate the performance of HRV in discriminating between groups with high and low risk of death. The standard deviation of five consecutive RR intervals (SDANN) was found to be the parameter with the greatest sensitivity (90%) and specificity (91%). Patients with SDANN values of < 55 msec had a twenty-fold increased risk of death (90% confidence limits: 4-118, P < 0.001). The results furthermore suggest that measurements of HRV are superior to other prognostic markers such as left ventricular ejection fraction, pulmonary artery wedge pressure, cardiac index, and serum sodium levels. We conclude that HRV is a powerful, noninvasive tool to assess the risk of death in candidates for HTX. HRV measurements can therefore be used as a supplement to other markers of risk to determine the optimal therapeutic strategy in patients with severe congestive heart failure.