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Ann Thorac Surg 1998;65:1703-1710
© 1998 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, University of Muenster, Muenster, Germany
b Department of Neurology, University of Muenster, Muenster, Germany
Accepted for publication February 19, 1998.
Address reprint requests to Dr Schmid, Department of Cardiothoracic Surgery, Albert-Schweitzer-Str 33, 48149 Muenster, Germany
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Abstract |
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Methods. Thirty-six patients underwent implantation of a Novacor N100 LVAS for various reasons. The surgical procedure was elective in 18 patients and scheduled on an urgent or emergency basis in another 18 patients. The assist period lasted from 17 to 336 days (109 ± 88 days); 22 patients were forwarded to heart transplantation after being supported for 140 ± 87 days.
Results. Clinical cerebral embolism was evident in 17 patients (47%). Thromboembolic events were singular in 8 and multiple in 9 patients; in the latter up to 10 TE occurred (mean ± SD, 1.4 ± 2 TE). Leading neurologic symptoms were unilateral hemiplegia in 11, as well as ocular symptoms and aphasia in 12 patients each. Noncerebral TE were detected in 4 patients, 2 of whom underwent an emergency operation for intestinal and iliac artery occlusion. The incidence of TE did not correlate strongly with the interval of LVAS support. Cerebral computed tomography confirmed lesions in 58% of patients. Transcranial Doppler sonography detected microembolic signals on 67% of all recordings, with the microembolic signals being more frequent on days with clinically manifest TE. The outcomes were good, as only 2 patients suffer from neurologic sequelae.
Conclusions. Thromboembolism is still a major threat for patients with LVAS implantation. Neurologic sequelae are frequent but have a favorable prognosis, and systemic complications occur considerably less often. Patient selection, adequate anticoagulation, and transcranial Doppler sonography may help to reduce the incidence of TE.
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Introduction |
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In view of this complication rate, we analyzed the incidence of neurologic events and thromboembolic complications in our patients with the Novacor N100 LVAS. In a subset of patients, we further visualized microembolic signals (MES), using serial transcranial Doppler (TCD) sonography as a means to improve patient surveillance [3]. Although these microemboli usually do not generate clinical symptoms, their predictive value for stroke has recently been demonstrated in patients with asymptomatic carotid artery stenosis [4].
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Material and methods |
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TopAbstractIntroductionMaterial and methodsResultsCommentReferences |
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Implantation technique and perioperative management
The assist devices were implanted during extracorporeal circulation with the heart beating as described previously [5]. The pump chamber was placed into the posterior sheath of the left rectal muscle and the diaphragm was partially detached from the rib cage to gain enough space for the conduits. The drive line was directed towards the right lower abdomen through a long subcutaneous tunnel to prevent infection. All patients were extubated as early as possible. Hemodynamic landmarks were pump volume more than 5 L/min, mean arterial pressure more than 80 mm Hg, and central venous pressure less than 20 mm Hg.
In all cases, anticoagulation was initiated and maintained by intravenous dextran and heparin until removal of all drains. An activated partial thrombin time of 60 to 80 seconds was considered adequate. This lasted 2 weeks or more, as in some cases considerable amounts of asanguineous effusions developed within the device pocket. Thereafter, oral anticoagulation was started using phenprocoumon, with a target international normalized ratio ranging between 2.5 and 3.5. Aspirin and dipyridamole or other platelet-inhibiting drugs were not routinely used in the early cases, when bleeding was the main concern. However, with increasing experience and repeated bouts of thromboembolism aspirin became a routine adjunctive in the last 7 patients.
The console-driven system was used only in the first patient. The wearable system (N100P) was available for the second patient and has been used exclusively since then. All inflow and outflow conduits were mounted with stented pericardial valves. In the first 12 patients, the commissural posts were not aligned to the conduit wall, resulting in hemodynamic dead space prone to thrombus formation. New inflow and outflow conduits without sinus of Valsalva were introduced in our institution in autumn 1994 (starting with patient 13) and implanted in all patients thereafter. The last 5 patients were provided with the next-generation LVAS, in which noise reduction was the most evident new feature (N100PC), starting in October 1996.
Transcranial Doppler monitoring and microembolic signal detection
A subgroup of 8 patients (starting with patient 12) underwent embolus detection by TCD for 30 minutes. Transcranial Doppler monitorings were performed using a pulsed Doppler sonography machine with a 2-MHz probe and a sample volume of 10 mm (Pioneer 4040, EME, Überlingen, Germany). The middle cerebral artery was identified and the probe was fixed to the temporal skull with an elastic band to minimize movement artifacts. During the entire monitoring period an experienced investigator was present to notice patient movements and to detect MES acoustically on-line. All recordings were stored on digital audio tapes for later off-line reevaluation (Fig 1).
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The patients were monitored daily during the first 30 postoperative days [7]. After this period, in these patients as well as in the following ones, an attempt was made to perform baseline bilateral TCD recordings the day before the operation, twice a week postoperatively in a prospective manner until a study end point was reached, and within 24 hours after occurrence of clinically manifest thromboembolic complications. The study protocol further included transthoracic echocardiography on days 14 and 30, as well as immediately after thromboembolic events.
Postoperative findings
Anticoagulation measurements were obtained serially to provide adequate anticoagulation in all patients. In case of manifest or suspected thromboembolism, a complete neurologic examination was obtained by a neurologist. An urgent cranial computed tomographic scan was performed to immediately exclude intracranial bleeding; a second scan followed within 5 to 7 days to confirm or exclude major cerebral ischemic lesions.
Findings at explantation, including thrombus formation in the LVAS, its conduits and sinus of Valsalva, as well as in the patient’s own heart, were noted at the time of LVAS explantation, ie, transplantation or death.
Statistical analysis
Statistical analysis of the data was performed with Statview (Abacus Concepts, Inc), an Apple/Macintosh-based computer program. Initially, all three groups were compared by an analysis of variance (ANOVA, parametric data) or Kruskall-Wallis (nonparametric data) test for the various parameters, where appropriate. Significant differences between two groups were then confirmed by an unpaired t test (parametric data) or Mann-Whitney U test (nonparametric data), respectively. Spearman’s rank test was applied to evaluate correlations. A value of p less than 0.05 was considered significant.
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Results |
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Embolic events
Embolism affected mainly the brain, whereas peripheral embolism occurred less frequently (in only 4 patients). Cerebral embolism was clinically evident in 17 (47%) patients. Embolic events were singular in 8 patients and multiple in 9 patients; in the latter up to 10 events occurred (mean ± standard deviation, 1.4 ± 2.0 events). Leading neurologic symptoms lasting for minutes, hours, or days included unilateral hemiplegia in 11, ocular symptoms (amaurosis fugax, anisocoria, paralysis of the oculomotoric nerve), and aphasia in 12 patients each. One patient each presented with absence and vertigo. In the surviving patient group, all symptoms resolved completely with time except in 2 patients. These patients still suffer from mild residual hemiplegia. Two further patients with complicated postoperative courses had development of hemiplegia and coma, were immobilized at the intensive care unit, and eventually died of multiorgan failure (Table 2).
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Computed tomographic findings
Computed tomographic scans were performed in all 17 patients with cerebral events. Cerebral infarcts were confirmed in 10 patients, with the ischemic areas being unilateral in 7 patients and bilateral in 3 patients. Mean age of the patients with and without radiologic evidence of thromboembolism did not differ (42 ± 14 versus 43 ± 10 years, NS). There was also no difference with respect to the underlying heart disease or cardiac arrhythmias. Eight patients had ongoing atrial fibrillation, but embolic events developed in only 3 of them; all of the latter events remained radiologically invisible. All patients with positive computed tomographic findings presented with sinus rhythm.
Transcranial Doppler sonography findings
Preoperative TCD monitorings were obtained in 6 of 8 patients and revealed MES (n = 2) in only one patient. All 8 patients showed MES during the LVAS period. During the cumulative follow-up of 990 days, 350 monitorings were performed, and MES were detected on 231 occasions (67%). Significant differences in the frequencies and numbers of MES were noted among the patients (both p < 0.05). Frequencies ranged from 38% to 100% and the medians ranged from 6 (95% confidence interval, 0 to 4) to 40 (95% confidence interval, 21 to 174). Early TCD monitoring revealed significantly higher MES numbers on days with clinically manifest embolism as compared with event-free days (8 [3 to 39] versus 4 [0 to 22], median [95% confidence interval]; p < 0.001). However, in contrast to our preliminary results, a critical threshold value of MES appearing in asymptomatic patients for occurrence of clinically manifest thromboembolic events could not be established.
Findings at explantation
Extensive thrombus formation within the left ventricle was found in only 1 patient. Thrombus formation in the LVAS was found in all 12 patients with the older type of valves. In these patients, vegetations consisting of thrombus material were attached to the valvular ring and the sinus of Valsalva of both the outflow and inflow tracts. No thrombus formation was evident within the pump chambers of these patients. After introduction of the new valves only 1 patient revealed thrombus material at the site of the LVAS. This was a rather small woman with peripartum cardiomyopathy, who was undersized for the device (153 cm; 35 kg; body surface area, 1.3 m2). At explantation, the whole inflow and outflow tract was covered with a thick layer of fibrous tissue on its luminal side. Similarly, no thrombus formation was present in the pump chambers [8].
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Comment |
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Thrombus formation and consecutive systemic embolism are consequences of the Virchow triad, which might be interpreted in LVAS patients to include artificial surface, blood stasis, and inadequate anticoagulation. The blood pump of the Novacor system has a one-piece seamless sac with a smooth polyether urethane blood-contacting surface designed to prevent adhesion of platelets and thrombus formation, respectively. This concept seemed to work out quite well; however, to some extent thrombus formation occurred in all patients with the early Novacor system. The heaviest deposits were seen by us and others on the silicone-flanged bovine pericardial valves, especially on the concave side of the inflow valve [14]. As a consequence, the valve design was changed in both the inflow and outflow tracts in 1994. Thereafter, no or only minimal thrombus formation was present at explantation of the device. Interestingly, the incidence of systemic embolization did not decline significantly in our experience; to our surprise, the incidence of neurologic events remained rather constant. As the native heart may also represent a source of thromboembolism—clots may form in ventricles with poor contractile function, in atrial fibrillation, and at artificial valves—intensive echocardiographic studies were performed. However, no thrombus material could be visualized within the patients’ hearts except for in the first patient.
Blood stasis in the recipient heart is also determined by the opening of the recipient aortic valve during support. In the standard fill-rate mode without a significant ejection delay the aortic valve is closed throughout systole. Only at a decreasing assist ratio or prolonged ejection delay can partial aortic valve opening be noted at rest [15]. We have chosen this mode in most patients to allow us to completely unload the heart and thus minimize myocardial stroke work. Intermittent opening of the aortic valve to clear the left ventricle was achieved on physical exertion, as tested by echocardiography [16]. Whether the asynchronous relationship of the native heart to LVAS ejection may also have implications for the blood flow pattern through both the native heart and the device is yet unknown. One might only speculate on whether an increased ejection delay of the LVAS would reduce embolism.
The intensity of anticoagulation is still a matter of discussion. Because both bleeding complications and thromboembolism may occur, anticoagulation must be adapted to the patient individually. As we experienced considerable bleeding problems from the unsealed conduits during our early experience, we did not use platelet inhibitors either alone or in addition to intravenous or oral anticoagulation in our early cases. Currently, our complication rate compares favorably with that of others in terms of bleeding problems and inadequate anticoagulation, early on as well as during longer periods of LVAS support [2, 17, 18]. Thus, we convert to phenprocoumon after 1 or 2 weeks, maintaining the prothrombin time at 1.5 times that of control (international normalized ratio, 2.5 to 3.5); we also administer aspirin. Low-molecular-weight dextran is added only during the first week. In this study, almost half of the events occurred while the patients were adequately anticoagulated, according to activated partial thrombin time and international normalized ratio. Our data indicate that these most frequently measured anticoagulant values alone are not sufficient as surveillance markers in this patient cohort.
Transcranial Doppler sonographic measurements did not correlate with the intensity of anticoagulation. However, our initial results suggest that serially performed MES detection by TCD can provide prognostic information on the individual risk of LVAS patients [7]. The predictive value of MES counts with regard to later manifest embolism was astonishingly high during the 30-day follow-up. This may suggest that part of the detected MES are not caused by full blood clots but rather reflect bubbles resulting from cavitation or other phenomena. The current data cannot rule out or confirm this assumption because we did not evaluate the whole panel of hemostasiologic measures. Platelet counts did not influence the amount of MES and thromboembolic complications in our patients, as has been previously reported [7]. One may further conclude that single microemboli are too small for manifestation of symptoms and remain clinically silent. This is in accordance with the fact that some patients showed some MES on TCD monitoring while being asymptomatic. However, a larger number of microemboli can cause vessel obstruction if they follow the same intracranial route. Siebler and colleagues [19] described this mechanism as the "traffic jam principle." Alternatively, one may hypothesize that an increase in Doppler MES may indicate a systemic prothrombotic state favoring the development of critical-sized macroemboli. Thus, these microemboli could serve as a surrogate marker indicating those patients with an increased risk of clinically manifest thromboembolism.
Systemic embolization is considerably less frequent, compared with cerebral embolism. However, even if there are probably many more asymptomatic emboli and infarctions, as has been recognized by imaging techniques, the sequelae of systemic embolism can be similarly serious. In our experience, arterial embolectomy caused by leg ischemia and small bowel resection because of occlusion of a mesenteric artery necessitated an emergency operation associated with an increased risk of bleeding complications because of consequent higher anticoagulation. It is questionable whether repeated abdominal and cerebral computed tomographic scans are justified to rule out asymptomatic embolism.
The complication rate is strongly related to patient selection. It is well known that patients of advanced age, those undergoing a repeat procedure, or those presenting with significant carotid stenosis are at increased risk for ischemic brain damage. In a heavily calcified aorta or carotid vessel, atherosclerotic plaques may loosen and embolize. Additional morbidity may affect bleeding complications, which require a lowering of effective anticoagulation. Regarding our still unsatisfactory complication rate, it must be kept in mind that we were dealing with an extremely ill patient cohort and that many of the adverse events reflect the learning process, when the possibilities and limits of LVAS use were still somewhat unclear. For example, in half of the patients, the LVAS was inserted under conditions of urgency or emergency. This special patient cohort is well known to have an increased risk, as coagulation disorders are common, optimal hemostasis is almost impossible, and infection problems are imminent [20]. We experienced rather extensive bleeding problems when implanting the LVAS for a failed routine operation with long periods of extracorporeal circulation or after extracorporeal membrane oxygenation implantation, the latter situation being very hazardous. Similarly, patients with acute low output after myocardial infarction usually present with abnormal coagulation after full heparinization or even intracoronary thrombolysis. In these patients, it also may be very difficult to attach the inflow conduit to the ventricular apex if the latter is partially necrotic as a consequence of the myocardial infarction. Moreover, the experience of a single case (patient 14) readily illustrates the consequences of a body size that is too small [8]. It is also noteworthy that additional morbidity may contribute to considerable complications in the postoperative course, as was seen in 2 of our patients who needed additional implantation of a cardioverter/defibrillator system.
Despite numerous investigations in patients with LVAS and artificial hearts, with thorough examination of platelet function, coagulopathy, fibrinolysis, and rheology, no antiembolic treatment protocol is safe so far, and thromboembolism remains a major problem. Embolic events may occur early after LVAS implantation, when it is difficult to balance the regimen of anticoagulation, and at a late stage, when patients tend to take less care of themselves. Our perioperative LVAS management includes routine anticoagulation measurements, cranial computed tomography, and TCD. Whereas cranial computed tomography allows visualization after cerebral embolism only at a late stage, TCD may be a useful adjunct for prevention [7]. Patient selection and adequate anticoagulation, including the use of platelet inhibitors and control of infection, may further help to reduce the incidence of thromboembolic events. Fortunately, severe complications with irreversible damage or ongoing disability of the patient are rare, and are attributed mainly to systemic embolization; most neurologic disorders, ie, hemiplegia, aphasia, or amaurosis, have an excellent prognosis. From our limited experience, we suggest that close surveillance of anticoagulation is of the utmost importance, and that TCD may help provide additional information for the risk stratification of future thromboembolic complications.
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