Surgical and mechanical support of the failing heart

The surgical treatment of acute heart failure is limited to cases of pressure or volume overload. Acute valvular regurgitation due to active endocarditis or to prosthetic dysfunction is a classic example of failure which can be cured by restoring valvular competence. Acute pressure load is mostly caused by prosthetic dysfunction or pulmonary embolism; therapy is aimed at removal of the causative agent. Coronary heart disease can cause heart failure by volume overload: acute mitral incompetence or ventricular septal defect lend themselves to surgical correction. In the surgical treatment of acute heart failure maximal attention is devoted to optimal timing of surgery, anesthetic management and postoperative care. Careful attention to the function of the right and left ventricle and combination of catecholamines, afterload reducing agents and volume loading together with respirator support have considerably improved the surgical results. Acute pump failure due to coronary insufficiency and infarction is less amenable to surgical treatment, with rare exceptions of emergencies during coronary angiography and percutaneous dilatation. The intra-aortic balloon pump is the only method of mechanical circulatory assistance which has reached widespread clinical acceptance. The best results are achieved in conjunction with surgery: either as cardiac support in inherently reversible postoperative heart failure or as the means of circulatory stabilization prior to surgery. Ventricular assist devices are still in the experimental stage: their use has been sharply curtailed by the virtual disappearance of the postoperative low output syndrome. In selected cases of end-stage cardiomyopathy cardiac transplantation is nowadays performed with acceptable survival (7O% at one year after surgery). Both orthotopic and heterotopic transplantation (transplanted heart in parallel with the natural one) give comparable results, but the procedure is still very restricted due to the lack of donors, multiple contraindications and lack of suitable heart preservation technique

Echocardiographic findings late after myectomy in hypertrophic obstructive cardiomyopathy

Postoperative echocardiograms of 50 patients undergoing myectomy for hypertrophic obstructive cardiomyopathy between 1965 and 1982 have been evaluated. In 21 patients a comparison with preoperative echocardiograms showed that postoperatively there was a significant reduction of septal and free wall thickness, an increase of left ventricular end-diastolic as well as outflow tract dimensions and a reduction or disappearance of systolic anterior motion of the mitral leaflet. Postoperative examination at intervals > 3 years revealed a significant increase of left ventricular and left atrial cavity size with unchanged contractile parameters and little reduction of left ventricular hypertrophy. In 4of 12 patients evaluated > 8 years after myectomy, left ventricular dilatation was observed and 3 of these 4 patients developed congestive heart failure. Development of leftventricular dilatation was independent of whether a transventricular and/or transaortic approach was used for myectomy. These data indicate that the late course after myectomy in hypertrophic obstructive cardiomyopathy may be complicated by dilatation of the left ventricular cavit

Valve replacement in octogenarians: increased early mortality but good long-term result

Between January 1983 and December 1990, 20 patients aged 80 years or older underwent valvular surgery. The patients' ages varied from 80 to 87 years (mean, 82 ± 1.5 years). The indication for operation was aortic stenosis in 19 patients, and mitral insufficiency after previous mitral valve replacement with a bioprosthesis in one. There were 15 elective, two urgent, and three emergency operations. Four of these patients had aortic valve replacement plus coronary artery bypass grafting. Six patients (30%) had an uneventful hospital stay, and the other 14 (70%) experienced several post-operative complications. The operative mortality rate was 15± (three patients). All patients before operation were in NYHA (New York Heart Association) class III and IV and all survivors remained in NYHA class I or II. The survivors have been followed from 6 to 70 months (mean 20 ± 8 months). The actuarial survival rate at 1 and 5 years was 78.5% and 67%, respectively. Valvular replacement in octogenarians can be performed, despite the high rate of post-operative complications, with increased but acceptable mortality. Long-term results are goo

Isolated aortic valve replacement with the Björk-Shiley tilting disc prosthesis and the porcine bioprosthesis

Between 1977 and 1978, 239 patients underwent aortic valve replacement with either a bioprosthesis (100, BIO) or a Björk-Shiley tilling disc prosthesis (139, BS). Early mortality was 2%, late mortality 4%. There was no statistically significant difference between the two groups. Anticoagulation was maintained indefinitively in patients with a BS, after implantation of a BIO only for three months except in the presence of atrial fibrillation or a history ofeinboli. Thromboembolic complications and anticoagulant hemorrhages were almost twice as frequent in patients with BS than with BIO (5.3 versus 2.8 episodes/100 patient years). This difference however is statistically not significant. There were an equal number (two) of reoperations because of paravalvular leaks due to endocarditis or torn sutures in the two groups. A regurgitant murmur, though hemodynamically not significant, occurred more frequently in patients with BIO than with BS (10% versus 2%, P < 0.05). Its cause and importance cannot yet be determined. Postoperative results judged by the NYHA classification and reduction of heart size were similar in both groups. Of all patients, 13% with preoperative valvular incompetence and 15% with stenosis showed little or no reduction of the cardiothoracic ratio on X-ray indicating a worse long-term prognosis. The porcine BIO has become our preferred valvular substitute because of its low thromboembolic complication rate. The BS is mainly reserved for patients already on anticoagulants for other reaso

Long-term outcome after traumatic anterior dislocation of the hip

Introduction: Traumatic anterior dislocation of the hip joint is rare. Additional injuries to the hip due to dislocation are even more infrequent. Outcome is limited by osteoarthritic joint degeneration or the occurrence of avascular necrosis of the femoral head. Method: Anterior hip dislocation occurred in ten of 100 patients with traumatic hip dislocations (8 men, mean age: 43, 22-62years) at two major trauma centres, between January 2001 and December 2008. Four patients had impaction fractures of the femoral head and three patients had fractures of the anterior acetabular wall. One patient presented with an open dislocation. In three of the ten patients surgical treatment was necessary. Results: Nine patients were evaluated retrospectively at a follow-up of 4.8±2.3years (mean±SD). The mean scores were 88±19 (Harris Hip-Score), 15±23 (WOMAC-Score), level 6 (UCLA-Score). Four cases presented with only fair clinical or radiological results according to Epstein. AVN with collapse of the femoral head was observed in one. Conclusion: Traumatic anterior hip dislocations presented in six of the ten cases with additional injuries to the hip. Surgical treatment in cases with deep impaction fractures of the femoral head or with large fragments of the acetabulum may improve the outcom

Physiologic or pathologic hypertrophy

Physiologic hypertrophy occurs as the result of exercise conditioning and is characterized by normal or supranormal left ventricular (LV) contractile function and reversibility of structural alterations. Whether hypertrophy produced by chronic abnormal loading can be termed ‘physiologic' is a matter of debate because in experimental pressure overload hypertrophy normal in vivo ventricular function may be associated with abnormal in vitro function of the papillary muscles. In patients with moderate LV hypertrophy from aortic valve disease (angiographic mass 20 mm Hg and/or cardiac index 2·5 l/mm/m2)interstitial fibrosis (IF) was increased to a similar extent (16 and 18%: normal <5%), whereas muscle fiber diameter (MFD normal ≤ 20 μ) was larger (P <0·05) in the patients with failure (30 μ) than in those with preserved function (27 μ). Moreover patients with depressed postoperative function had a larger (P < 001) preoperative MFD (35 μ) than those with normal postoperative function (30 μ). Seventeen months after successful aortic valve replacement IF increased (P < 0·02) and MFD decreased (P < 0·001) but did not become normal regardless whether postoperative function was normal or depressed. Thus in secondary hypertrophy myocardial structure is pathologic even in the presence of normal LV function and depressed function appears likely to be related to excessive fiber hypertrophy rather than to IF. Massive fiber hypertrophy heralds an unfavorable postoperative LV function and fibrosis is irreversible after surgical correction of the abnormal loa

Myocardial function and structure in aortic valve disease before and after surgery

Left ventricular (LV) micromanometry, cine-angiography and endomyocardial biopsies were performed in 13 patients with aortic valve disease {AVD) before and 12 to 28 months after successful valve replacement. (AVR). Patients with coronary artery disease were excluded. In nine patients (Group I: five AS, four AI) postoperative LV ejection fraction (EF) and total pressure Vmax were normal(EF ≥ 0.61; Vmax ≥ 1.50 ML/s). In four patients (Group II: three AS, one AT) postoperative EF (0.41) and Vmax (1.21 ML/s) were depressed. Pre-operative muscle fiber diameter (MFD; normal < 20 n) was 31 μ in Group I and 38 μ in Group II (P < 0.01). After AVR MFD decreased to 27 μ in Group I (P < 0.005) and to 28 μ in Group II (P < 0.02). Prior to surgery EF and Vmax showed no significant correlation with the LV fibrous content (FC in g/m2; FC = interstitial fibrosis in percent × LV angiographic muscle mass/100) in the 13 patients with AVD. After AVR, however, FC was related inversely to EF (P < 0.01, r = −0.69) and to Vmax (P < 0.025, r = −0.63). It is concluded that: (1) in AVD massive pre-operative fiber hypertrophy heralds impaired postoperative LV function; (2) fiber hypertrophy regresses following AVR regardless of the-LV functional state, and (3) the content of fibrous tissue appears to be a determinant of postoperative LV functio

Predictability of aortic dissection as a function of aortic diameter

The role of aortic diameter on the occurrence of type A dissection was investigated in 73 patients with dilated ascending aorta at the lime of pre-operative evaluation. Using transthoracic echocardiography for diagnosis and measurements, 54 patients were identified with type A dissection (group 1) and 19 without dissection (group 2). The true mean aortic diameters were identical (6·0±1·3 cm in group 1 and 6·4±1·4 cm in group 2; mean±SD; ns) as were the indexed aortic diameters (ratio of diameter/body surface area; 3·2±0·8 cm . m−12 and 3·4±0·7cm m−2 respectively; ns). However, the individual diameters showed a pronounced scatter in both groups (range from 3·6±11·0 cm). Of the 73 patients, 66 had surgery (47/54 with and 19/19 without dissection) and seven patients were treated medically. Emergency surgery was performed in 45/66 patients (all with acute type A dissection) andelective repair in 21/66 (19 without and two with chronic type A dissection). In-hospital mortality was 18% in the emergency group, 5% in the elective group and 57% in the medical group. It is concluded that patients with dilated ascending aorta have a substantial incidence of acute dissection. Their clinical course is unpredictable; acute dissection occurs in some, and in others the ascending aorta continues to enlarge without dissection. Because patients with dissection often arrive too late for elective repair andhave to be operated on as emergencies with a higher operative risk, we recommend elective surgery before the diameter of the ascending aorta has reached 6 c

Left ventricular relaxation at rest and during handgrip in aortic valve disease before and after valve replacement

In 14 patients (pts) with aortic valve disease (A VD) left ventricular (LV) relaxation was assessed by the time constant (T) of LV pressure (tipmanometer) fall before and 19 months after successful aortic valve replacement (A VR). 12 control pts (CO) were studied by the same technique. Preoperative LV ejection fraction in AVD (64%) and in CO (69%) did not differ. In AVD T was increased (60 ms) as compared to the CO (38 ms, P< 0.05). During handgrip (HG) there was a similar increase of LV peak systolic pressure (LVSP), heart rate and peak measured contractile element velocity of shortening in A VD and in the CO. L V end-diastolic pressure varied minimally in both groups. T decreased during handgrip in CO (38 to 33 ms, P<0.01) and remained unchanged in A VD. Following AVR T at rest decreased insignificantly to 52 ms, but remained increased (P<0.025) as compared with CO. During postoperative HG however, a decrease to 47ms (P<0.05) was noted. Postoperative angiographic LV muscle mass (105 g/m2) and LVSP at rest (137 mmHg) remained elevated (P<0.02) as compared to CO (72 g/m2; 119 mmHg). It is concluded that (1) in A VD with normal ejection performance L V relaxation at rest is prolonged and the reaction of relaxation to HG is abnormal despite preserved contractile response, (2) following A VR the response of LV relaxation to HG becomes normal and (3) elevated postoperative T at rest appears to be related to residual hypertrophy and probably also to the still increased LVSP rather than to intrinsic disturbances of myocardial relaxatio