Author + information
- Received December 7, 2010
- Revision received April 21, 2011
- Accepted May 10, 2011
- Published online September 13, 2011.
- Shahbudin H. Rahimtoola, MB, FRCP, Dsc (Hon)⁎ ()
- ↵⁎Reprint requests and correspondence
: Dr. Shahbudin H. Rahimtoola, University of Southern California, 1200 North State Street, Old General Hospital, Room 3221, Los Angeles, California 90033
This review covers the period from July 2009 to June 2010, with 3 exceptions.
Statin does not reduce the progression of mild-to-moderate aortic stenosis
Two hundred sixty-nine patients with mild-to-moderate aortic stenosis (AS) were randomized to 40 mg of rosuvastatin or placebo (the ASTRONOMER [Aortic Stenosis Progression Observation: Measuring Effects of Rosuvastatin] trial) (1). At a median follow-up of 3.5 years, there was no significant difference between the 2 groups in the progression of severity of AS.
Natural history of “very severe” AS
Consecutive asymptomatic patients (age 67 ± 16 years; women 57 years) were followed clinically with “very severe” AS (2) defined as peak aortic valve jet velocity (AV-Vel) ≥5.0 m/s; aortic valve area (AVA) was 0.63 ± 0.12 cm2. During a median follow-up of 41 months, 96 events were observed, which included aortic valve replacement (AVR) in 90 patients and 6 cardiac deaths that occurred in previously asymptomatic patients (sudden 1, heart failure 4 [causes of heart failure was not given], myocardial infarction 1). Event-free survival at 1, 2, 3, 4, and 6 years was 64%, 36%, 25%, 12%, and 3%, respectively. The AVA for patients with AV-Vel >5.5 m/s and 5.0 to 5.5 m/s were not statistically significantly different. Patients with AVA by echocardiography of <0.6 cm2 had a similar outcome to those with AVA ≥0.6 cm2. Coronary artery disease (CAD) was present in 22%; the number of patients who had coronary arteriography was not provided.
This study of 116 patients, from 1995 to 2008, was labeled as “very severe” AS.
Did these patients have “very severe” AS? The AVA was 0.63 ± 0.12 cm2, and the event rate at 1 and 2 years was 36% and 64%, respectively. A previous study from the same institution of 128 patients, obtained during 1 year (1995), reported on patients with “severe” AS in whom the AVA was 0.69 ± 0.1 cm2 (range was 0.4 to 0.8 cm2), and the event rate at 1 and 2 years was 36% and 54%, respectively (3). Another study also reported 66 patients with “severe” AS who had no CAD on coronary arteriography in whom the AVA was 0.61 ± 0.17 cm2 and the event rate at 1 and 2 years was 43% and 62%, respectively (4). Thus, there is not much difference in AVA and event rates between patients with “very severe” and “severe” AS. Also in this study there was no significant difference in outcomes between those with AVA <0.6 and ≥0.6 cm2, because both had severe AS.
So, what is “very severe” AS? The concept of “very severe” AS was presented in the 2006 Denolin lecture at the European Society of Cardiology Annual Congress (5) on the basis of the study of Amato et al. (4) (as AVA ≤0.7 cm2) and that of Braunwald's (6) “critical” obstruction to left ventricular (LV) outflow (as aortic valve area index [AVAI] of ≤0.4 cm2/m2). The AV-Vel/peak gradient by Doppler echocardiography occurs in early systole, and the problems are: 1) the severely stenotic aortic valve is not fully open at that time (7); 2) even in normals (animal/human), LV emptying in early systole is by the phenomenon of mass acceleration (8,9), which results in an increased velocity/gradient that is increased by sympathetic/inotropic stimulation—gradients as high as 55 mm Hg have been documented (10); and 3) gradients/velocities are movable targets (11), except with “critical AS” (also see grading severity of AS in the following text).
Grading severity of AS is inconsistent
The grading of 333 consecutive patients who underwent cardiac catheterization was evaluated (10). The criteria of mean pressure gradient (MPG) >40 mm Hg for severe AS was inconsistent with criteria of AVA calculations in 26% of the patients. To document that a low cardiac output was not the cause of the inconsistency, they evaluated the influence of flow, assuming normal stroke volume of >35 ml/m2, which is lower than the stroke volume in normal people (in whom it is 45 ± 10 ml/m2) (12).
The authors previously documented similar inconsistencies with echocardiography/Doppler data (13). These investigators have made a major contribution to properly assessing severity of AS.
Using MPG >40 mm Hg as a criteria to indicate that AS is severe, as was done in the guidelines, is the problem. In the guidelines the Level of Evidence: C was used in 75% to 91% of the recommendations, indicating that it was based on “opinions.” The origin and source of this criterion is uncertain. Gradient is a per-beat function that is dependent on LV loading conditions and contractility and also on the pressure in the ascending aorta (AA) (11); it can frequently be changed rapidly. In 636 patients undergoing cardiac catheterization, MPG ≥50 mm Hg was specific with 90% or more positive predictive value for severe AS (14), but MPG <50 mm Hg had low specificity for severe AS and was consistent with severe as well as not-severe AS. A modification of the figure of the authors (Fig. 1) confirms this earlier data; of interest, the majority of patients with MPG <50 mm Hg had severe AS.
Data from 1,563 patients in the SEAS (Simvastatin and Ezetimibe in Aortic Stenosis) study (15) from echocardiographic/Doppler studies showed that pressure recovery adjusted AVAI (energy loss index) (16) obtained at the sinotubular junction would allow “for accurate assessment of AS severity.”
The best method to assess severity of AS is the energy available to perfuse the body (Effective Energy Requirement), which is determined after Conservation of Energy (12). At the present time, determination of whether AS is severe should be based on an assessment of the combination of clinical criteria plus AVAI at cardiac catheterization/energy loss index at the sinotubular junction by echocardiography/Doppler of ≤0.6 cm2/m2 and/or MPG ≥50 mm Hg (12–14), and determination of critical/very severe AS should be based on AVAI of ≤0.4 cm2/m2 (5,6,12).
Long-term survival after AVR in very elderly persons (age ≥80 years) is similar to that of the general population
Of 7,584 consecutive patients, 51.1% had AVR and 48.9% had AVR + coronary artery bypass graft surgery (CABG) (17). Their actuarial survival was similar to the life expectancy of the general population obtained from actuarial tables, which at ages 80 to 84 years is 7 years and at age ≥85 years is 5 years.
Extent of pre-operative myocardial fibrosis influences the extent of functional improvement after AVR in symptomatic patients with severe AS
Fifty-eight consecutive patients with isolated symptomatic severe AS had extensive baseline characterization before AVR that included cardiac magnetic resonance imaging (MRI) (late-enhancement imaging for fibrosis) (18). Endomyocardial biopsies were performed intraoperatively to determine the extent of fibrosis. The extent of histologically determined fibrosis at baseline was similar to that determined by MRI and correlated with New York Heart Association (NYHA) functional class (FC). Nine months post-operatively, late enhancement was unchanged. The amount of fibrosis determined the NYHA FC improvement.
This is an interesting and important study.
Persistent diastolic dysfunction late after AVR in severe aortic regurgitation is due to persistently increased muscle fiber diameter, interstitial fibrosis, and fibrous content
Eleven patients with severe aortic regurgitation (AR) were studied before, early (21 months), and late (89 months) after AVR with LV biplane angiograms, high-fidelity pressure measurements, and LV endomyocardial biopsies (19). Fifteen healthy persons served as control subjects but did not have endomyocardial biopsies.
In patients with AR, LV volumes and mass were increased; and after AVR were reduced, LV mass decreased but did not become normal. Left ventricular ejection fraction (LVEF) was reduced and improved after AVR. Myocardial fibrosis and the increased constant of muscle stiffness were increased and remained increased late after AVR and accounted for persistent diastolic dysfunction.
This is an important and valuable study.
Bicuspid Aortic Valve
Vascular dysfunction in those with dilated AA
Thirty-two men with nonsevere AS were separated into 16 subjects (Group A) with nondilated AA (≤35 mm) and those with dilated AA (n = 16, Group B) and were compared with 16 healthy men (control subjects, Group C) (20). Despite similar degrees of AS, LV mass, and function, those in Group B had significantly higher plasma levels of matrix metalloproteinases, higher carotid-femoral pulse wave velocity, and blunted brachial flow-mediated vasodilatation to hyperemia, compared with those in Group A.
Statins reduce progression of mitral stenosis?
From an echocardiographic database of 20 years, 315 patients who had mitral stenosis (MS) (61 ± 12 years of age, 71% female) were evaluated; follow-up was 61 ± 4 years (21). Thirty-five patients (11.1%) had been treated with statins. The average rate of progression was 0.062 ± 0.079 cm2/year. Fast progression, defined as annual change in mitral valve area (MVA) >0.08 cm2/year, was present in 3 of 35 (8.6%) patients who had received statins versus 83 of 280 (29.6%) who had not received statins (p = 0.008).
Pre- and post-procedural mitral regurgitation is associated with poorer outcomes after catheter balloon commissurotomy for MS
Patients (n = 876) undergoing their first catheter balloon commissurotomy (CBC) were separated into 3 to 5 subgroups according to mitral regurgitation (MR) grades (22). In hospital and on late follow-up (mean 4.11 years), the incidence of composite endpoints was greater in those with MR (Table 1).
Open heart surgery versus CBC in MS: similar survival but better event-free survival with open heart surgery
One hundred fifty-nine patients (52 ± 9 years of age) underwent open heart surgery, and 402 (44 ± 1 years of age) had CBC from 1995 to 2000 (23); their echocardiographic scores were 9.6 ± 1.9 and 7.3 ± 1.4, respectively, p < 0.001. Follow-up was 106 ± 27 months (median 109 months). At 9 years, adjusted cardiovascular death-free survival was similar (96 ± 2% vs. 95 ± 2%), but adjusted probability of clinical event-free survival was greater with open heart surgery (94 ± 1% vs. 80 ± 2%; p = 0.0001).
Increased stress and myofibrillar degeneration in isolated MR with LVEF >0.60
Twenty-seven patients (age 53 ± 12 years) with isolated severe MR and LVEF 0.66 ± 0.05 who had no obstructive CAD, MS, or aortic valve diseases had cardiac catheterization and were compared with 39 “normal subjects,” 40 ± 11 years of age. Of the MR patients, 45% were in NYHA FC I, and 55% were in FC II (24). After mitral valve repair (MVrep), there were significant decreases of LVEF (0.66 ± 0.05 to 0.54 ± 0.09, p < 0.0001) and of LV end-diastolic volume index (108 ± 28 to 78 ± 24, p < 0.05); the increased left ventricular end-systolic volume index was unchanged. The LV circumferential and longitudinal strain rates were reduced after MVrep. The LV end-systolic stress/LV end-systolic volume index were depressed at baseline and after MVrep when compared with normal subjects (0.25 ± 0.10 and 0.28 ± 0.25 versus 0.33 ± 0.12, p < 0.01). The LV myocardial biopsies demonstrated myofibrillar degeneration versus control subjects (p = 0.035); biopsies in control subjects were obtained in 7 young subjects who died of noncardiac disease. Patients with MR also showed increased xanthine oxidase (p < 0.05) and lipofuscin deposition (p < 0.01). The authors concluded that: 1) decreased strain rates and LV wall stress/LV end-systolic volume index after MVrep “indicate contractile dysfunction despite pre-surgical LVEF >0.60”; and 2) the “increased oxidative stress could cause myofibrillar degeneration and lipofuscin accumulation resulting in LV contractile dysfunction in MR.”
This is an innovative and important study. It would have been valuable to know whether the patients in NYHA FC I had findings identical or similar to those who were in FC II.
Suboptimal reproducibility of quantitative measurements of severity of MR
Eighteen echocardiographers from 11 academic institutions in Israel, Japan, and the United States evaluated the same images from 16 patients with MR (25). The overall interobserver agreement for grading MR as severe or not severe for jet-area-based MR grade was 0.32 (95% confidence interval [CI]: 0.1 to 0.52), for vena contracta was 0.28 (95% CI: 0.11 to 0.45), and for proximal isovelocity surface area was 0.37 (95% CI: 0.16 to 0.58).
Exercise echocardiography for all asymptomatic patients with severe degenerative MR? Not yet
Sixty-one asymptomatic patients with moderate-to-severe MR had rest and bicycle exercise Doppler-echocardiography (26). Note that: 1) effective regurgitant orifice area by proximal isovelocity surface area and Doppler provided different values; 2) the same was also true for regurgitant volumes—mean values by the 2 techniques differed both at rest and on exercise by an average of 20 ml; 3) “there were no significant exercise-induced changes in regurgitant volume”; and 4) the regurgitant volume and LV outflow tract stroke volume were stated to be 77 ± 22 ml and 81 ± 23 ml, respectively, even though the LV end-diastolic volume was only 111 ± 35 ml! The findings on exercise are similarly discordant (see Table 2 of the authors ).
This study is from an experienced center. Nevertheless, were serious methodological issues involved in the measurements that were made?
Improvement of moderate MR with isolated CABG for symptomatic left main or 3-vessel CAD? Yes, in the presence of hibernating myocardium and less LV dyssynchrony
Of 135 patients undergoing CABG, operative mortality was 4.4%, late deaths amounted to 6.2%; and 121 survived to 12-month follow-up. All patients had left main CAD or proximal 3-vessel CAD (27). Indications for CABG were symptoms (NYHA FC 2.5 ± 0.9), angina in 81%, and extent of CAD; grafted vessels averaged 3.5 ± 1.4, 79% had a previous myocardial infarction. Dysfunctional but viable myocardium (hibernating myocardium) was diagnosed by a perfusion-metabolism mismatch on single-photon emission computed tomography, dyssynchrony by tissue Doppler imaging (TDI). At 12-month follow-up, 57 (47%) showed no or mild MR (“Improvement” group), and 64 (53%) showed no improvement of MR (“failure” group); at baseline there were no significant differences between the 2 subgroups. At follow-up the “improvement group” had significant reductions of LV end-diastolic and end-systolic volumes and increase of LVEF from 0.35 ± 1.0 to 0.47 ± 0.09, p < 0.0001. The independent predictors of improvement were ≥5 segments with viability and absence of dyssynchrony. Of patients with viability in ≥5 segments and dyssynchrony of <60 ms, 93% improved. In the “failure group” 18% and 34% of those with nonviable myocardium and dyssynchrony improved and 49% and 32% showed worsening of MR, respectively (p < 0.001). The clinical outcome was significantly better in the “improved group” (Fig. 2).
Rigid prosthetic ring annuloplasty has the best but unsatisfactory results for secondary tricuspid regurgitation
From 1990 to 2008, 2,277 patients underwent tricuspid valve procedures at the time of aortic and mitral valve procedures (28). At 3 months, no tricuspid regurgitation (TR) was present in only 32% and 3+/4+ TR was present in 11%. By 5 years, no TR had decreased to 22% and 3+/4+ TR had increased to 17%. Patients with rigid ring annuloplasty had the least increase of 3+/4+ TR to 12% at 5 years.
Very good results of tricuspid valve surgery for secondary TR are still awaited.
Early surgery for valve endocarditis is associated with a better survival
Native Valve Endocarditis: A Prospective Multinational Study of 1,552 Patients
Seven hundred twenty patients (46%) underwent early surgery, and 832 (54%) had only medical therapy (29); early surgery was associated with significantly lower mortality (12.1% vs. 20.7%, p < 0.001). After propensity matching and adjustments for survivor bias, the absolute risk reduction was −5.9% (p < 0.001), which increased to −11.2% (p < 0.001) with “instrumental-variable-mortality reduction” (Table 2). In subgroup analysis, surgery conferred a survival with absolute risk reductions of −10.9% with propensity matching for surgery, −17.3% in those with paravalvular complications, −12.9% in those with systemic embolization, −20.1% in those with Staphylococcus aureus infection, and −13% in those with stroke but not those with valve perforation or heart failure.
An excellent accompanying editorial discusses the difficulties of analyzing the complexity of this problem (30).
Prosthetic Valve Endocarditis
Of 133 cases of prosthetic valve endocarditis, 24 (18%) were early onset (<60 days after valve implantation) and 109 (82%) were late onset (≥2 months) after valve implantation (31).
Staphylococci were the most common organisms (72%) in early onset; in late onset, staphylococci and streptococcus viridans were the cause in 29% and 19%, respectively.
Complications occurred in 16 of 24 (66.7%) of early prosthetic valve endocarditis and in 80 of 109 (73.4%) of late onset.
Hospital mortality was 29.3%. There were a number of comorbid conditions that were predictors of mortality. The 12-month survival in the medical and medical-surgical groups was 42% and 71%, respectively (p = 0.007). In the Cox regression analysis, surgical treatment was a significant factor in better survival (odds ratio: 0.43, 95% CI: 0.24 to 0.75, p = 0.003). There was no significant difference in survival in the early and late onset groups.
Allografts (homografts) and mechanical prosthesis for aortic native valve endocarditis
One hundred thirty-eight patients underwent AVR in 2 centers, 106 received homografts (age 47 years, range 14 to 76 years), and 32 received mechanical prostheses (MP) (age 47 years, range 16 to 75 years) (32). Abscess was present in 38% of homografts and in 8% of MP. Hospital mortality was 8% (9% with homografts and 3% for MP, p = 0.25). At 15 years, survival and recurrent endocarditis were better for MP (p = NS). Hazard ratios of structural valve deterioration (SVD) for homografts in the first 5 years, 5 to 10 years, 10 to 15 years, and 15 to 20 years were 0.23%, 0.82%, 1.0%, and 6.7%/patient-year, respectively. Reoperation rate was lower for MP (7 ± 6% vs. 24 ± 9%, p = 0.02).
Transcatheter Valve Therapy: Aortic Valve
Randomized trial: transfemoral transcatheter valve therapy is associated with better survival than with “standard therapy” (PARTNER [Randomized Placement of Aortic Transcatheter Valves] trial)
Of 3,105 patients with AS, 12% (358) who were considered to be “not suitable for surgery” were randomized to transcatheter valve therapy (TVT) with Sapien valve (Edwards Lifesciences, Inc., Irvine, California) or no prosthetic heart valve (PHV) (n = 179 in each group) (33). Patients were 83.1 ± 8.6 years of age, 92% were in NYHA FC III/IV with Society of Thoracic Surgeons (STS) Score of 11.2 ± 5.8 and AVA of 0.6 ± 0.2 cm2.
At 30 days, TVT versus “standard therapy” was associated with all-cause mortality of 5.0% versus 2.8% (p = 0.41), stroke/transient ischemic attack 6.7% versus 1.7% (p = 0.03), vascular complications 30.7% versus 5.0% (p < 0.001), and major bleeding of 16.8% versus 3.9% (p < 0.001). The statistically significant differences at 1 year are shown in Figure 3 and Table 3.
This is an important landmark randomized trial. Nevertheless, certain aspects of the trial need to be noted. First, 83.8% of patients in the “standard therapy” group had aortic balloon valvuloplasty. This procedure was shown in 1994 in the large National, Heart, Lung, and Blood Institute Registry to be ineffective (34) and thereafter was abandoned. The 2000 and 2006 guidelines give it a Class III grade for calcified valves. To consider it as “standard therapy” was very controversial from 2007 to 2009. It is also known to produce AR (34). The incidence of moderate or severe transvalvular AR in the “standard therapy” group was 16.9% versus 1.3% in the TVT group. This is in addition to 11% incidence of paravalvular AR. This amount of acute AR (27.9%) in the LV of severe AS can be a problem (34). Second, 12 patients in the “standard therapy” group had standard surgical AVR. Their 1-year death rate was 33%, which is similar to the 31% death rate at 1 year in the TVT group. Should the subjective classification of “cannot undergo surgery”/“not suitable candidates for surgery” be re-evaluated? Third, deaths from unknown cause were assumed to be deaths from cardiovascular causes. The numbers of such deaths in each group were not provided and depending on the number of such deaths in the “standard therapy” group the conclusion(s) of this trial could be impacted. Fourth, subgroup analysis for death from any cause was not significant in those with body mass index ≤25 kg/m2, LVEF >0.55, oxygen-dependent chronic obstructive pulmonary disease, pulmonary hypertension, and peripheral vascular disease.
Other issues include: 1) at 30 days the complication rate is higher in the TVT group; 2) from Figure 3 it seems that at 6 months there was no significant difference between the 2 groups for death from any cause and death from any cause or major stroke; 3) at 1 year, several complications were much higher in the TVT group; and 4) the multivariate predictors of death and/or stroke were not provided.
However, this is an early stage of TVT. Improvements in the devices, procedures, and patient selection will occur in the ensuing years.
Transapical TVT in patients with severe AS at high risk at a single center
One hundred seventy-five patients 79.8 ± 9.0 years of age, with STS Score 23.5 ± 19.4, AVA 0.57 ± 0.22 cm2, 98.3% in NYHA FC III/IV, 5.7% in cardiogenic shock, and LVEF <0.35 in 22.8% had transapical (TA) TVT with the Sapien valve (Edwards Lifesciences) in a single center in a hybrid operating room by a team of physicians (cardiac surgeons, cardiologist, and anesthesiologists) (35). Technical success was 100%; 30-day mortality was 5.1% (30% in those in cardiogenic shock, and 3.6% in the remaining patients). Survival at 1, 6, and 12 months was 94.9%, 85.5%, and 82.6%, respectively.
The authors emphasized the importance of training and coordination between members of the team.
TA and transfemoral TVT for AS
In the multicenter Canadian study of 339 patients, 168 had the transfemoral (TF) and 177 had the TA procedure (36). The AVA was 0.63 ± 0.17 cm2, 90.9% were NYHA FC III/IV, 69% had CAD, estimated glomerular filtration rate <60 ml/min was present in 56.3%, and porcelain aorta was present in 17.9%. The STS score was 9.8 ± 6.4%; the procedural success rate was 93.3%. The 30-day mortality in TF and TA was 9.5% and 11.3%, respectively. After a median follow-up of 8 months, mortality was 22.1%.
The predictors of cumulative late mortality were peri-procedural sepsis or need for hemodynamic support, pulmonary hypertension, chronic kidney disease, and chronic obstructive pulmonary disease.
One hundred fifty-three patients had TVT by the TF route, and 50 had TVT by the TA route; their STS scores were 6.5 ± 4.1 and 6.3 ± 3.8, respectively (37). Patients who had TVT by the TF and TA routes had similar NYHA FC (3.1 ± 0.3). Patients in the TA group were more frequently women; had higher B-type natriuretic peptide values and smaller AVA; and had more CAD, peripheral arterial disease, and kinking of the descending aorta. Despite baseline differences, survival was similar. Some complications were specific to the access site.
The authors emphasized that TF is the procedure of first choice and TA was chosen only in patients who had no access through diseased femoral arteries.
Cerebral emboli after TF TVT for AS
Thirty-two patients who had TVT for AS were evaluated (38); 27 (84%) had multiple new foci of restricted diffusion on cerebral MRI and, such foci occurred in 48% of a “control” group who had surgical AVR. There were 1 to 19 lesions/patient; the lesion volume was 77 mm2 (range 59 to 64 mm2), whereas in the surgical group the lesion volume was 224 mm2 (range 111 to 338 mm2). There were no measurable impairments of neurocognitive function and no apparent neurological events. The MRIs at 3 months showed no change.
Thirty patients were evaluated; 20 completed the protocol of 3 MRI images (39); 16 of 22 (72.7%) had 75 new cerebral lesions after TVT; 3 of 30 (10%) had new neurological findings, and 1 (3.6%) had a permanent neurological impairment. The National Institutes of Health Risk Score and serum concentration of neuron-specific enolase were not correlated with MRI findings.
Valve prosthesis-patient mismatch after TVT for AS with Medtronic core valve
Valve prosthesis-patient mismatch (VP-PM) occurred in 16 of 50 patients (32%). The VP-PM was moderate (PHV area ≤0.85 cm2/m2) in 15 and severe (PHV area ≤0.65 cm2/m2) in 1 patient (40). Optimal position defined as optimal device depth 5 to 10 mm occurred in 50% of patients. The incidence of VP-PM was 16% in the optimal position and 48% in the nonoptimal position (p = 0.015).
Prosthetic Heart Valves
Randomized trial: MP versus bioprostheses in patients 55 to 70 years of age
Power calculations estimated approximately 155 patients were needed in each group to have 80% power (a beta error of 20%) to detect a 10% difference in mortality and for 2-sided alpha error of 5%.
Over an 8-year span (1995 to 2003), of 1,120 patients who needed AVR, 155 were randomized to MP and 158 were randomized to bioprostheses (BP) (41). At late follow-up (106 ± 28 months), there was no statistically significant difference in the primary endpoint of survival (Fig. 4); however, at 12 years there were only 12 and 16 patients at risk in the BP and MP groups. In the primary endpoints of valve failure (SVD) and reoperation, the differences in valve failure (linearized rate) in BP was 2.17% patient year (95% CI: 1.35 to 2.95) versus 0 in MP (p = 0.0001), and the differences in reoperation in BP was 2.32% per patient year (95% CI: 1.48 to 3.18) versus MP 0.62% per patient year (95% CI: 0.19 to 1.05) (p = 0.0003). There were no significant differences in the secondary endpoints.
First, the duration of follow-up in the study was not adequate for a full appreciation of the extent of SVD in the BP. Second, the final results are similar to the Edinburgh (42) and Veterans Administration trials (43), which had follow-up of 20 and 18 years, respectively, and average follow-up was 15 years. Nevertheless, the major finding of considerable interest and value of this trial is that “newer” PHV (BP and MP) had no different outcomes compared with the “older” PHV that were used in Edinburgh and Veterans Administration trials.
Choice of PHV in adults
An updated comprehensive review can be seen in Rahimtoola (44).
10- to 15-year survival after AVR plus MVR in patients <70 to ≥80 years
One thousand fifty-seven patients had surgery from 1989 to 2007 in Northern New England (45).
Data are from the Social Security Administration Death Master File. An AVR was performed in 98.1% (tissue valve in 64.7% and mechanical in 35.4%), MVR was performed in 60.5% (of whom 51.2% had tissue valve, 48.8% had mechanical valve), and MVrep was performed in 39.5%. “In-hospital” mortality for those age <70, 70 to 79, and ≥80 years was 11%, 18%, and 24%, respectively. Mean survival was 7.3 years (Table 4).
Accelerated streptokinase is not better than standard infusion for left-sided PHV thrombosis: a randomized trial
Of 120 patients, 60 received accelerated streptokinase infusion (1.5 million units [MU] of streptokinase) over 1 h, and 60 received conventional infusion (0.25 MU over 30 min) (46). In both groups streptokinase was continued at 0.1 MU/h infusion up to 72 to 96 h. There were no statistically significant differences with regard to complete clinical response, composite secondary outcome or major bleeding. The success rate was low (59%) and worst in those in NYHA FC III/IV (Table 5).
Valve Prothesis-Patient Mismatch
VP-PM determined 6 months after AVR is associated with increased mid-term cardiac-related mortality
Six hundred forty-five consecutive patients 72.3 ± 7.9 years of age had AVR between 2000 and 2007 and had indexed PHV area (effective orifice area index) at 6.5 ± 1.5 months determined by echocardiography/Doppler (47). A VP-PM was defined as PHV area <0.85 cm2/m2. The PHV areas were presented for 8 different PHVs. For the 8 valve brands for each valve size, there was a range of actual PHV sizes that were obtained in patients (see Table 2) in their report ); one such example is shown in Table 6. Follow-up times were mean 2.66 (median 2.35, range 0.45 to 7.19) years. A VP-PM was associated with a higher incidence of cardiac death (Fig. 5). Predictors of cardiac death were smaller PHV size, age, diabetes, and preoperative LVEF <0.50.
This is another important and valuable study of VP-PM from the German Heart Center group in Munich.
SVD of the “stenosis type” in BP is related to VP-PM
Five hundred sixty-four patients, 74 ± 5 years of age, had received 9 different brands of BP at a median follow-up of 6.1 years (maximum 16.4 years) (48). Structural valve deterioration was diagnosed in 40 (7%), “stenosis type” was diagnosed in 24, and “regurgitant type” was diagnosed in 16 patients. Patients with VP-PM (PHV size <0.85 cm2/m2, n = 285) developed SVD that was “stenosis type” and started to occur after 2 to 3 years. Patients without VP-PM developed SVD of the “regurgitant type,” which started to occur after 9 years. Multivariate analysis showed PHV size ≤21, and VP-PM were predictors of increased SVD. Anticalcification treatment administered during valve preparation was a predictor of a lower incidence of SVD.
This is another excellent and careful study by Professor Flameng. The accompanying editorial by Carpentier, who introduced the term “bioprostheses” in 1969 for glutaraldehyde-processed animal valves, is excellent and discusses the issue of SVD (49).
Pericardial effusion after cardiac surgery with cardiopulmonary bypass
Of 21,416 patients operated from 1993 to 2005, 327 (1.5%) had pericardial effusion, 272 (83%) of whom had only valve surgery. It was diagnosed at 9 ± 6 (median 7) days, moderate or large effusion was seen at 13 ± 6 days (50). Two hundred eighty patients (86%) had nonspecific symptoms (Table 7), and 138 (42%) had cardiac tamponade. It was recurrent in 4%. Independent risk for effusion after valve surgery had an odds ratio of 3.7 (95% CI: 2.6 to 5.2, p < 0.0001).
This is a necessary and very valuable study. In much earlier times this was called the “post-pericardiotomy syndrome.” It might occur after hospital discharge, and the clinical presentation is nonspecific. It is important to recognize and treat this uncommon complication in a timely fashion, because it can be life-threatening with development of cardiac tamponade and occasionally results in “late” development of constriction.
Dr. Rahimtoola has received honoraria for educational lectures from the American College of Cardiology Foundation; American College of Physicians; University of California Los Angeles; University of California Irvine; Cornell University; Creighton University; Thomas Jefferson University; Cedars-Sinai Medical Center; Harvard Medical School; University of Wisconsin; University of Hawaii; Cardiologists Association of Hong Kong, China; University of California, Fresno; ATS; St. Jude Medical; Carbomedics; Edwards Lifesciences; Merck; and Pfizer.
- Received December 7, 2010.
- Revision received April 21, 2011.
- Accepted May 10, 2011.
- American College of Cardiology Foundation
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