YEAR IN CARDIOLOGY SERIES
The Year in Valvular Heart Disease
Shahbudin H. Rahimtoola, MB, MACP, MACC, DSc(Hon), FRCP*
Division of Cardiovascular Medicine, Department of Medicine, LAC+USC Medical Center, Keck School of Medicine, University of Southern California, Los Angeles, California
Manuscript received September 22, 2005;
accepted November 9, 2005.
* Reprint requests and correspondence: Dr. Shahbudin H. Rahimtoola, Distinguished Professor, University of Southern California, 2025 Zonal Avenue, Los Angeles, California 90033.
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Heritable component of Valvular Heart Disease (VHD)
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The Utah Population Database is a population-based genealogical resource composed of Utah pioneers and their descendants that contains electronic records of 2,237,324 individuals. The familial relative risk of death for age <65 years was four times higher in first-degree relatives of those with aortic valve disease (Table 1) (1).
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Atherosclerosis, calcification, and bone formation in valves
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Calcific aortic stenosis (AS).
Early lesions are similar to atherosclerosis, with prominent accumulation of "atherogenic" lipoprotein, including low-density lipoprotein (LDL) and lipoprotein(a), evidence of LDL oxidation, an inflammatory cell infiltrate, and microscopic calcification. In late lesions, there are more prominent accumulation of lipid cells and extracellular matrix (Fig. 1) (2).
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Figure 1 (A) Potential pathways depicting calcific aortic valve disease. IL = interleukin; TGF = transforming growth factor; and MMP = matrix metalloproteinase. (B) Histological findings in early and late lesions of calcific aortic valve disease. In early lesion, arrow indicates displacement of normal subendothelial elastic lamina. In late lesion, arrow indicates elastic lamina is displaced and fragmented. (Verhoeff-van Giesen stain, original magnification x100). From Freeman and Otto (2). Prints of figure provided by C.M. Otto, MD.
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Mitral valve.
Rabbits fed a 1.0% cholesterol diet showed an increase in connective tissue and collagen formation, increased myofibroblast proliferating cell nuclear antigen-staining and alpha-actin-positive staining cells, macrophages, significant deposition of osteopontin, and increased levels of osteopontin ribonucleic acid expression. Rabbits fed cholesterol and atorvastatin showed markedly lower atherosclerotic lesions (Fig. 2) (3).
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Figure 2 Light microscopy of rabbit mitral valves and papillary muscle. Control diet, cholesterol, and cholesterol + atorvastatin. All frames, magnification x12. (A) Alpha-actin immunostain, (B) RAM-11, macrophage immunostain, (C) Proliferating cell nuclear antigen, (D) Masson trichrome stain, (E) Osteopontin immunostain. From Makkena et al. (3). Prints of figure provided by N.M. Rajamannan, MD.
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Rheumatic valves.
Calcification within the rheumatic valves was not seen in degenerative or normal valves. Vascular endothelial growth factor was present in areas of inflammation. Immunohistochemistry localized osteopontin and osteocalcin to areas of smooth muscle cells within microvessels and proliferating myofibroblast, and their protein expression was upregulated in the calcified rheumatic valves (Fig. 3) (4).
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Figure 3 Identification of bone matrix markers in calcified human rheumatic valves. Stains as in Figure 2. C = osteocalcin immunostain. Arrow points to myofibroblast staining cells (magnification x40). All others, magnification x10. Micro CT 3D reconstruction of calcified rheumatic valve (D1) and uncalcified degenerative mitral valve (D2). From Rajamannan et al. (4). Prints of figure provided by N.M. Rajamannan, MD.
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Aortic stenosis
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Cardiovascular magnetic resonance imaging (CMR) in AS.
The intra- and interobserver variability of aortic valve area (AVA) by CMR ranged from –0.18 to +0.13 cm2 and from –0.11 to 0.16 cm2. Patients underwent CMR 7 ± 5 days after cardiac catheterization (CC; n = 39); 10 ± 8 days after transthoracic echocardiography (TTE; n = 41); and 5 ± 5 days after transesophageal echocardiography (TEE; n = 35). The sensitivity and specificity to detect AVA  0.8 cm2 by CC for CMR was 78% and 79%; for TTE was 74% and 67%, and for TEE was 70% and 70% (5).
Comment
There was a time delay between CMR and other tests, but the procedural reproducibility of CMR was not documented. Performance of CC may have been less than ideal because aortic pressure was measured by "pull back;" also, the method of determining oxygen consumption is not given. Sensitivity and specificity to detect AVA 1.0 cm2 is not given but would have been of value to know.
Where is end-systole in aortic pressure tracing to assess AVA?.
Animal experimental AS showed the location of end of systolic outflow at the incisura may occur after left ventricular (LV) pressure has fallen below aortic pressure, at times called "hang out." It occurs for a minuscule period of time (18 ms) at a time when the flow rate is very small (<10 ml/s). In patients, depending on whether one uses the pressure crossover or at the incisura to calculate systolic ejection period, the flow rate and pressure gradient were different. In 38 patients, the values for AVA for the pressure crossover and incisura methods were 0.9 ± 0.33 versus 0.88 ± 0.36; the value for absolute difference in AVA was very small (0.02 ± 0.02) (6).
Comment
In the example provided, the LV and aortic pressures are less than satisfactory (Fig. 4).
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Figure 4 (A) Adapted from Bermejo et al. (6). Pressure tracings obtained with 8-F double lumen catheter. Both lumens, especially the aortic one, are very small. Both left ventricular (LV) diastolic and aortic pressure pulses look damped. Lumen of the aortic opening is about 15 to 20 cm from the LV opening and is frequently in the arch. There is a large "hang out." (B) Simultaneous LV and aortic pressure from two separate catheters in patient with severe aortic stenosis. Note the LV diastolic pressures are not damped, and the ascending aortic catheter, which is about 1 to 2 cm above the valve, shows "hang out" is very brief and minimal. The ascending aortic pressure shows the anacrotic "notch" on the ascending limb. Tracings provided by Anil Mehra, MD, Director, Interventional and Alex Durairaj, MD, Director, Cardiac Catheterization Laboratory, LAC+USC Medical Center. AVA = aortic valve area; AVAI = aortic valve area index; SEP = systolic ejection period.
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B-type natriuretic peptide.
B-type natriuretic peptide (BNP) was regulated by systolic and diastolic load, suggesting that myocardial stretch modulates BNP (7).
Induction of local angiotension II-producing system.
Angiotensin-converting enzyme (ACE) and chymase, two angiotensin-forming enzymes, are present in aortic valves and are upregulated in AS valves (8).
Weights of aortic valves to severity of AS.
Three hundred twenty-four patients had "isolated" aortic valve replacement (AVR) for AS, had peak LV to systemic arterial peak systolic pressure gradients  10 mm Hg, and had calculated AVA. As the weights of the valves increased from 1 g to >6 g, the average peak gradient increased and AVA decreased; the r values between the valve weight to gradient ranged from 0.49 to 0.62, and to AVA ranged from –0.28 to –0.44 (9).
Comment
Peak gradients were measured from LV to "systemic" arterial pressure and not to ascending aortic pressure; mean gradients are not presented. The r values were small. The method of measurement of cardiac output is not described. Aortic valve replacement was performed in many patients with moderate AS, in some with mild AS, and in one with minimal AS (AVA >2.0 cm2)!
Outcome of 622 asymptomatic adults with "hemodynamically significant" AS.
The authors stated, "The purpose of the present study was to evaluate the natural history of asymptomatic, hemodynamically significant valvular AS ..." (10). Six hundred ninety-four patients aged 40 years with valvular AS fulfilled entry criteria; 72 patients had AVR initially, and the remaining 622 formed the study group. During follow-up, 297 developed symptoms but 90 (30%) did not have surgery, and 325 remained asymptomatic but 145 (45%) had surgery. The probability of remaining free of cardiac symptoms while unoperated was 82% at one year, 67% at two years, and 33% at five years. At 10 years, there were six patients at risk.
Comment
Can one evaluate the natural history when there were no uniform criteria by which to perform or deny surgery in the asymptomatic and symptomatic patients? The incidence of performances of coronary arteriography and of associated significantly obstructive coronary artery disease (CAD) in patients who were aged 72 ± 11 years is not provided. In the Otto study (11), 42% of asymptomatic patients subsequently underwent coronary arteriography, and 50% of these had significantly obstructive CAD, including left main and three-vessel CAD. In the present study, were cardiac symptoms and events due to AS and/or CAD? Of interest, mortality of those undergoing surgery versus no surgery in those who developed symptoms was 21.7% versus 77.7%, and in those who remained asymptomatic 28% versus 57%; time from onset of symptoms to surgery and from symptoms and/or surgery to death is not provided.
Do pharmacological agents reduce progression and/or severity of AS?.
Beta-blockers, ACE-I, and angiotensin receptors blocks do not do so (12,13). A retrospective study suggested statins do (13); a randomized trial was negative (14).
Heyde’s syndrome.
Of 3.8 million patients discharged from public hospitals in the Republic of Ireland, the incidence of gastrointestinal bleeding in the presence of AS was 0.9% with an odds ratio of 4.5, 95% confidence interval (CI) 3.0 to 6.8, and a p value of <0.0001 (15).
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Aortic Regurgitation (AR)
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AV repair (AVrep) for AR.
Aortic valve repair was performed in 57% of patients undergoing surgery for AR. Hospital mortality was 3.9% (16); reoperation for recurrent AR was 3.3%. In patients with isolated repair, isolated root repair, and a combination of both, at five years the incidence of AR grade II was 19%, 16%, and 6%, respectively; the incidence of reoperation was 7%, 5%, and 2%, respectively.
Effectiveness of beta-blockade in experimental "chronic" AR.
Thirty-eight 38 male Wistar rats were studied (17). Metoprolol treatment, compared to no treatment, resulted in a smaller increase in LV size, prevented reduction of left ventricular ejection fraction (LVEF), increased the expression of B1-adrenoreceptor messenger ribonucleic acid, and reduced G-protein receptor kinase 2 levels. Collagen I and III in ribonucleic acid levels were reduced. Cardiac myocyte hypertrophy was also reduced.
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Bicuspid Aortic Valve (BAV)
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Aortic root dilation.
In 162 consecutive patients with BAV, age 23.6 ± 19.8 years (18), the dimensions at the sinuses of Valsalva, sinotubular junction, and ascending aorta were increased (Table 2).
AVrep for AR.
Of 132 patients with BAV + AR, 57% had AVrep and 43% had AVR (19). By multivariate analysis, AVrep was associated with eccentric jet direction, cusp thickening, commissural thickening, and cusp calcification.
Comment
There are no data on patient outcomes at follow-up.
Valve-sparing aortic root replacement by the remodeling technique: a "reasonable option?".
This procedure was performed in 60 patients with BAV (Group A) and in 130 patients with tricuspid aortic valve (Group B) (20). Comparing Group A to Group B, hospital mortality was 0% versus 5%; at five years, freedom from AR grade 2 was 4% versus >17% (p = 0.07), and freedom from reoperation was 98% versus 98% (Fig. 5).
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Figure 5 (A) Actuarial freedom from aortic regurgitation grade II after aortic root remodeling in bicuspid and tricuspid valves. (B) Actuarial freedom from reoperation. From Aicher et al. (20).
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Mitral Stenosis (MS)
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Catheter balloon commissurotomy (CBC) during pregnancy.
Thirty-six patients, age 25.8 ± 4.3 years, underwent CBC at a mean gestational period of 26.5 ± 5.3 weeks; 25 patients were in New York Heart Association (NYHA) functional class III/IV (21), 23 had a Massachusetts General Hospital (MGH) echocardiographic score of <8, and 13 had a score >8. Fluoroscopy time was <2 min in 8.3%, 2 to 4 in 55.6%. The procedure was successful in 35 of 36 patients with reduction of left atrial (LA), pulmonary artery (PA) pressures, and an increase of mitral valve area (MVA) from 0.74 to 1.59 cm2 (all p < 0.001). Mitral regurgitation (MR) increased by two grades in 19.4%; none needed valve surgery. There were no abortions or stillbirths; all children did well long-term and had normal mental development. All patients were in NYHA functional classes I and II.
Tricuspid regurgitation (TR) regresses after CBC.
Of 53 patients with severe MS and TR grade 2, on a 1 to 3 scale, TR regressed after CBC in 51% (22). Patients in whom TR regressed were younger and had lower incidence of atrial fibrillation (AFib), higher PA pressure, higher prevalence of functional TR, and more severe MS (p < 0.005).
Better LV function with chordal preservation at time of MVR for rheumatic mitral valve disease (MVD).
Patients who had complete chordal preservation (n = 250) on follow-up had smaller LV end-diastolic and end-systolic volumes and higher LVEF than those who had complete excision of subvalvular apparatus or who had preservation only of posterior chordopapillary apparatus (23). The last group had better LVEF than those who had complete excision of subvalvular apparatus.
Magnetic resonance imaging (MRI) for estimation of severity of MS.
In 17 patients the MVA by MRI showed a "good" correlation with CC (n = 17; r = 0.89) and a reasonable one with TTE (n = 20; r = 0.81) (24).
Predicting mean PA wedge pressure from Doppler recording.
Two-dimensional Doppler and tissue Doppler imaging were performed simultaneously with right heart catheterization in 51 consecutive patients (aged 64 ± 11 years) with MVD: 35 with moderately severe to severe MR and 16 with moderate to severe MS (25). The ratio of isovolumic relaxation time (IVRT) to TE-Ea for MR and for MS had r values of –0.92 and –0.88, respectively, both p < 0.001. The ratio of IVRT to  had r values of –0.74 for MR and –0.85 for MS (both p < 0.001).
Comment
In patients with MR, IVRT/TE-Ea of 15, the mean PA wedge pressure ranged from about 15 to 38 mm Hg, and in MS with IVRT/TE-Ea of 4.5, mean PA wedge pressure ranged from about 15 to 36 mm Hg. For MR for an IVRT/ of about 1.2 to 1.8, the mean PA wedge pressure ranged from about 10 to 25 mm Hg, and in MS for an IVRT/ of 1.2 to 1.6, mean PA wedge ranged from 16 to 32 mm Hg. All cited values are from a review of their Figures 3 and 4.
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Mitral regurgitation
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Acute pulmonary edema (APE) with ischemic mitral regurgitation (IMR).
Of 28 patients aged 65 ± 11 years with IMR, those with episodes of APE (Group I) were compared to 46 patients without history of APE, all of whom had previous acute myocardial infarction and LV systolic dysfunction (26). On exercise, patients in Group I had less reduction of LV end-systolic volume (p = 0.06), less reduction of LV wall motion index (p = 0.02), and greater increases of tenting area, regurgitant volume, effective regurgitant orifice area, and tricuspid pressure gradient (all p < 0.001).
AFib after MV repair (MVrep)/MVR is common.
Of 762 patients in sinus rhythm and with no previous history of AFib who had MVrep/MVR, 69 (9%) developed early AFib without recurrence (Group I); 67 (8.8%) had early AFib and also had late AFib at 10 years (Group II); and 44 (5.8%) developed only late new AFib (Group III) (27). Group I patients were characterized by angina class and lower LVEF, but not by LA enlargement (LAE), which was diagnosed as LA dimension 50 mm. Sixty-seven of 136 (49%) of those with early AFib developed late AFib. Large LA size independently predicted early AFib (p = 0.01) and late AFib (p = 0.003). Postoperative AFib was associated with an increased higher risk of stroke or heart failure (HF) (adjusted risk ratio 1.46; 95% CI 1.04 to 2.05; p = 0.03). The authors concluded that for patients with LA enlargement, "... surgery may be considered earlier in the course of the disease."
Comment
This was an interesting study. Patients with late AFib had higher systolic and diastolic blood pressure. Only 10% of those with late AFib had an "ischemic" etiology; 31% had MVR, of whom 47% had mechanical valves; there is no information on preservation of chordo-papillary apparatus (see the previous text); also, was rheumatic another etiology? Left atrial dimensions were not corrected for body size; the American Society of Echocardiography recommends maximum LA diameter in the A-P view 2.0 cm/m2 (36 ml/m2) as normal. The exact number of patients who initially had LAE can be calculated. It is stated that of patients with LAE, 20% (n = 136) developed early AFib; thus about 680 patients probably had LAE and 111 had late AFib, which is 16% (111 of 680). Surgery in 680 patients to save 111 from having late AFib puts 569 patients at risk for mortality and morbidity both early and late after surgery. Also, the incidence of late AFib was about 2% per year (12% at 5 years, 19% at 10 years). Aggressive treatment of co-morbid conditions and anticoagulation for late AFib is important but is not described. In the Atrial Fibrillation Follow-up Investigation of Rhythm Management study, larger LA diameters were associated with recurrent AFib (p = 0.01) but not with stroke (p = 0.44) (28); patients had warfarin with an international normalized ratio (INR) goal of 2 to 3. Moreover, in the current era catheter ablation of AFib is possible.
Asymptomatic patients with MR.
Four hundred fifty-six (456) asymptomatic patients (LVEF 0.70 ± 0.08%), 63% men, with organic MR were studied (29). The estimated five-year survival (±SE) of death from any cause, death from cardiac causes, and cardiac events (death from cardiac causes, HF, or new AFib) with medical management were 22 ± 3%, 14 ± 3%, and 33 ± 3%, respectively. Independent determinants of survival were increasing age, the presence of diabetes, and increasing effective regurgitant orifice (ERO). Those with ERO 40 mm2 when compared to those with ERO of <20 mm2 had increased event rates. Two hundred thirty-two patients had surgery: 94 for symptoms, 91 for echo parameters, and 47 by physician and patient preferences. Those who had surgery had better outcomes. The authors concluded, "patients with an ERO of 40 mm2 should promptly be considered for cardiac surgery."
Comment
The accompanying editorial (30) pointed out some of the limitations with regard to the conclusion and recommended a randomized trial of surgery on the basis of ERO. Earlier, Robert L. Frye, the most senior cardiologist at the Mayo Clinic and past president of the American College of Cardiology (ACC), had recommended a randomized trial of surgery in asymptomatic patients with severe MR (31). The cardiac causes of death averaged 3% per year, but was MR the cause of death? Patients’ age was 63 ± 14 years, but there are no data on the percentage of patients who at entry had coronary arteriography and significantly obstructive CAD. Important details of "medical management," for example, actual treatment and effectiveness of therapy of co-morbid conditions such as hypertension, were not provided. Twenty percent of those who had MVR/MVrep had surgery by physician and patient preferences.
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Tricuspid regurgitation
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Pulmonary thromboendarterectomy (PTE) reduces/abolishes pulmonary hypertension (PHTN) and severe TR.
Twenty-seven patients with severe TR underwent PTE; TR resolved in 19 (70%) (Group A) and was persistent in 8 (30%) (Group B) (32). By echo/Doppler, Group A patients had greater reduction of PA systolic pressure than Group B (85 ± 16 mm Hg to 36 ± 8 mm Hg vs. 87 ± 29 mm Hg to 55 ± 26) (p = 0.019) (Fig. 6). By cardiac catheterization data, the fall in PA systolic pressure was also greater in Group A than in Group B (37 ± 16 mm Hg vs. 16 ± 13 mm Hg; p = 0.004). No difference was observed in tricuspid annular diameter, apical displacement of the tricuspid valve, or other features between the two groups. The authors concluded, "After significant PA pressure reduction by PTE, severe functional TR with a dilated annulus may improve without annuloplasty despite dilated tricuspid annulus diameters."
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Figure 6 Preoperative and postoperative severity of pulmonary hypertension (by echocardiographic measurements) stratified by resolved (open bars) or persistent (solid bars) tricuspid regurgitation before and after pulmonary thromboendarterectomy (PTE). PAS = pulmonary artery systolic pressure. From Sadeghi et al. (32).
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Comment
These findings are impressive and suggest an important role for PTE early when TR is mild or even earlier when PHTN is moderate or severe.
Damage to tricuspid valve (TV) by permanent pacemaker (PPM) or implantable cardioverter-defibrillator (ICD) lead.
Of 41 patients, 7 had perforation of TV by PPM or ICD leads, 4 had lead enlargement of the TV, 16 had lead impingement of TV leaflets, and 14 had lead adherents to TV (33). The septal leaflet was perforated in six of seven cases. Transthoracic echocardiography diagnosed 12% of patients with TV leaflet perforation or impingement, and 63% of patients were diagnosed as having severe TR. Transesophageal echocardiography showed TV malfunction due to PPM lead in 45% and severe TR in all. Time from PPM implantation to operation was 72 months (range 2 to 228 months).
TV tethering predicts residual TR after tricuspid annuloplasty.
Two hundred sixteen patients with functional TR had two-dimensional TTE before and 5 ± 4 days after TV annuloplasty and left heart valve surgery (34). Multivariate analysis showed age, tethering distance, and severity of preoperative TR (all p < 0.001) were independent predictors of residual TR. The sensitivity and specificity in predicting residual TR after surgery were 86% and 80% for tethering distances <0.76 cm and 82% and 84% for tethering areas <1.63 cm2.
TR due to flail TV leaflets: medical and surgical outcome.
In 60 patients with TR due to "flail leaflets" (35), the most common cause was trauma (n = 37), of which 19 were due to blunt trauma and 18 to iatrogenic chordal severing, most from RV biopsy. Survival at 10 years was 61 ± 10%. Tricuspid surgery was performed in 33 patients at five years in 55 ± 7%. The composite event rate of dyspnea or HF, new AFib, cardiac surgery, or death at 10 years was 75 <13%.
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Sports activities for patients with VHD
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The ACC Bethesda Conference has made suggestions (36).
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Infective Endocarditis (IE)
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American Heart Association (AHA) scientific statement.
Describes recommendations for the diagnosis, anti-microbial therapy, and management of IE (37).
Molecular approach to diagnose IE.
Broad-range polymerase chain reaction (PCR) targeting bacterial and fungal rDNA followed by direct sequencing was applied to 52 excised heart valves with suspected IE and from 16 patients without any sign of IE. The sensitivity, specificity, and the positive and negative predictive values for the bacterial broad-range PCR were 41.2%, 100%, 100%, and 34.8% (38).
Comment
The accompanying editorial (39) describes the strength and weakness of this study.
Maximum of three TEEs is necessary for diagnosis.
Two hundred sixty-two patients with 266 episodes of suspected IE were referred for TTE/TEE (40). Of these, 47.8% had definite IE, 30.4% had possible IE, and in 21.8% the diagnosis was rejected. Diagnostic findings from TTE and TEE in the first examination were 21.2% and 68.5%, respectively; reclassifications after the second examination were 13.5% and 46.9%, respectively, and after the third examination were 7.5% and 20%, respectively. After the third examination, the yield was zero.
Antibiotic prophylaxis: better education needed.
The Euro Heart Survey on Valvular Heart Disease (41) documented antibiotic treatment was started before blood cultures were obtained in 71% of patients with IE. Fifty percent of those with native VHD had been educated in endocarditis prophylaxis, and 33% regularly attended dental follow-up. Only 50% of patients with IE who had had a procedure at risk during the preceding year had received adequate prophylaxis. The authors concluded: "... Improvement of patient management through education and implementation of guidelines ..." is justified.
Poor mid-term outcome for medically successfully treated IE.
Sixty-seven of 151 (44%) patients with IE were successfully treated (42). Thirty-five underwent late surgery to correct sequelae of the infection, and 21 of 35 (68%) of those who underwent late surgery died during follow-up. Forty patients (60%) died from cardiovascular causes as a direct consequence of IE or because of worsening of the underlying cardiac disease. Survival rates without cardiac surgery at 1, 3, and 5 years were 54%, 29%, and 20%, respectively.
Long-term results of MVrep.
Thirty-seven consecutive patients (43) underwent MVrep in "active endocarditis" using Carpentier’s techniques between 1989 and 1994; operative mortality was one (3%), and one patient had reoperation for pericardial patch dehiscence. At 10 years, survival was 80% and freedom from MV reoperation was 91%.
MVrep versus MVR: 154 patients underwent surgery between 1980 and 1996 (44); 63% had MVR and 37% had MVrep. The 30-day mortality was 3.2%; 4% after MVR and 1% after MVrep. Survival at 1, 5, and 10 years was 93%, 81%, and 61%, respectively; survival at 10 years tended to be better with MVrep (p = 0.15). Patients who had undergone MVrep were less frequently in NYHA functional classes III/IV (0% vs. 29%; p = 0.002), had a lower incidence of AFib (29% vs. 47%; p = 0.04), tended to have less dyspnea (20% vs. 38%; p = 0.07), and needed reoperation less frequently (1.8% vs. 6.5%).
Cryopreserved aortic valve homograft for active aortic IE.
From 1992 to 2002 (45), 104 patients had cryopreserved aortic valve homograft; 73% had IE of native valve, 27% for prosthetic valve; 80% had isolated aortic IE. Hospital mortality was 5%. At 10 years, actuarial survival rate was 83%, freedom from reoperation was 76%, and freedom from recurrent IE was 93%. There were no thromboembolic complications.
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Anticoagulant and anti platelet therapy
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Warfarin dose requirement is related to gene encoding vitamin K epoxide reductase complex 1 (VKORC1).
Ten common non-coding VKORC1 single-nucleotide polymorphisms were identified and five major haplotypes were inferred. A low-dose haplotype group (A) and a high-dose haplotype group (B) were identified (46). The maintenance dose (mean ± SE) of warfarin differed among the three haplotype group combinations (p < 0.001) (Fig. 7). Vitamin K epoxide reductase complex 1 haplotype Groups A and B explained approximately 25% of the variance in dose. The frequency of Group A haplotypes predictive of lower warfarin dose was higher in the Asian Americans (89%) and lower in the African Americans (14%) than in the European Americans (37%) (p < 0.001 for both comparisons). The group distribution (A or B) was also different between these populations. Thus, the molecular mechanisms of warfarin dose response appear to be regulated at the transcriptional level.
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Figure 7 Mean warfarin doses according to VKORC1 haplotype combination (A/A, A/B, or B/B) in all patients and in those with wild-type and variant CYP2C9. From Reider et al. (46).
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Antiplatelet plus moderate-intensity anticoagulation is the most effective?.
The National Study for Prevention of Embolism in Atrial Fibrillation, a prospective, randomized, open-label study, was performed in 13 hospitals (47). Patients with chronic or paroxysmal AFib were included; those at low risk were excluded. At high risk were patients with MS with or without prior embolism. These patients were randomized to anticoagulation with acenocoumarol (international normalized ratio [INR] range 2 to 3) or a combination of trifusal 600 mg (equivalent to aspirin 300 mg) and INR 1.4 to 2.4. Primary outcome was a composite of vascular death, transient ischemic attack, and non-fatal stroke or systemic embolism. The combined therapy group had fewer primary events, a log hazard ratio of 0.51, a 95% CI 0.27 to 0.96, and a p value of 0.03.
Comment
The accompanying editorial cautioned that the authors’ conclusion that in the combination therapy the lower limit of an INR of two is the safe limit is premature (48).
Aspirin or warfarin after AVR with biological prosthetic heart valve (PHV).
Patients undergoing AVR with biological PHV received warfarin (n = 41, INR between 2 and 3) or aspirin 100 mg/day (n = 108) by surgeon’s choice (49). During the first three months, there was no statistically significant difference between the two groups with regard to cerebral ischemic events, major bleeding events, stroke-free intervals, and overall survival.
Between 1993 and 2000, 1,151 patients underwent AVR with bioprosthesis. By surgeon preference, 624 had early postoperative anticoagulation (AC+) and 529 did not (AC–) (50). Operative mortality was 4.1%. Postoperative cerebrovascular accident occurred in 2.4% of the AC+ group and in 1.9% of the AC– group. The incidence of cerebral events at <30 days in the AC– group was 1.5%. The incidence of re-exploration for bleeding in the AC+ group was 5.0% and in the AC– group was 7.4% (p = 0.085).
Comment
Seventy-eight percent of patients in the AC– group received antiplatelet therapy. Thus, both of the above studies did not evaluate the role of antiplatelet therapy versus placebo.
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Percutaneous heart valve procedures
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Percutaneous mitral annuloplasty (PMA) for MR in experimental HF (51).
Study 1
Percutaneous mitral annuloplasty, using a novel annuloplasty device with two anchors, reduced annular dimension and severity of MR at baseline and after phenylephrine infusion to increase afterload. Pressure volume analysis demonstrated no acute impairment of LV function.
Study 2
Seven animals were studied four weeks after device placement for HF. The mitral annulus decreased from 3.75 ± 0.08 to 3.37 ± 0.23 (p < 0.05), and the severity of MR was reduced (MR jet area/LA area from 0.33 ± 0.03 to 0.11 ± 0.04; p < 0.05).
Society of Thoracic Surgeons (STS)/American Association for Thoracic Surgery/Society for Cardiovascular Angiography and Interventions position statement (52).
The recommendations were endorsed by the ACC and AHA.
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Special surgical situations
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Limited durability of valve repair in patients with previous mediastinal radiation therapy.
Twenty-two patients age 61 ± 14 years underwent valve repair, 15 ± 9 years after mediastinal radiation therapy (53). Follow-up was 3.7 ± 3.3 years. "Early" mortality was 14%. Of 19 early survivors, overall survival, freedom from cardiac death, and freedom from valve reoperation or cardiac transplantation at five years were 66%, 85%, and 88%, respectively.
Surgery in octogenarians.
Aortic valve replacement for severe AS ± coronary artery bypass grafting (CABG): One hundred fifteen patients aged 82.3 ± 2.1 years underwent AVR (62%) or AVR + CABG (38%). Aortic valve area was 0.62 ± 0.15 cm2 (54). Hospital mortality was 8.5%. The five-year survival was 69.4%. At five years the survival for patients with bioprosthesis was 81.7% versus 56.7% with a mechanical valve (p = 0.02). Predictors of late mortality were LVEF (p < 0.01), preoperative HF (p < 0.03), and the type of prosthesis (p < 0.03). Preoperatively, 79% were in NYHA functional classes III to IV. Postoperatively, 94% were in classes I to II.
Valve surgery ± CABG: In 405 patients, several different procedures were performed (55). "Early" mortality was 6.4% and ranged from 0% to 10%; it was 4.3% for AVR and 8.2% for AVR + CABG; 5.7%. for MVR/MVrep ± CABG. At five years, survival after AVR was 66 ± 5%; after MV surgery, 68 ± 9% (p = 0.12). Concomitant CABG did not affect late survival. Independent predictors of late death were age 85 years and LVEF 0.40. At a median follow-up of two years, NYHA functional class was improved: preoperative 78% classes II to IV and 18% class I; postoperative 72% class I and 17% class II.
Surgery for isolated non-rheumatic MR: Fifty-nine patients, age 80 years or older (82 ± 2 years), had first-time MVrep (n = 46) or MVR (n = 13). The etiology was "degenerative" in 95% (56). Operative mortality was 1.7%. The five-year survival was 61%. Preoperatively, 79% were in NYHA functional classes III/IV; postoperatively, 78% were in NYHA functional classes I/II.
Improved patient outcomes with hybrid approach.
Twenty-six patients, median age 72 years (range 53 to 91 years) had percutaneous coronary intervention and within a median of 5 days (range 0 to 14 days) underwent primary or reoperative valve surgery (57). Patients were at high risk with an expected STS-predicted mortality of 22%. With the hybrid approach, the operative mortality was 3.8% and the median blood loss 900 ml, and 22 patients (85%) required blood transfusions. Survival rates at one, three, and five years were 78%, 56%, and 44%, respectively.
Euro score for predicting late mortality.
One thousand one hundred five operative survivors who had undergone isolated valve surgery ± CABG were studied (58); the five-year mortality (by Euro score) is shown in Table 3.
Operative mortality of MR surgery with LVEF 0.30.
An STS database of 14,582 patients showed operative (30-day) mortality for patients with LVEF 0.30 (n = 727) versus LVEF >0.30 (n = 13,855) was 5.4% versus 3.1% (p = 0.001). Low LVEF was not a significant factor for mortality after controlling for other factors (59). In patients with LVEF >0.30 versus 0.30, mortality after MVrep was 1.4% and 1.53%, respectively, and after MVR was 7.69% and 10.18%, respectively.
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Prosthetic heart valves
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Starr-Edwards PHV is durable for more than 40 years.
Since 1960, the Starr-Edwards valve has been used in 3,653 of 8,300 PHVs that were inserted by Starr and his colleagues. The original models had "some engineering" alterations up to 1964. In 1965, the models A1200/A1260 and M6120, called "extended-cloth prosthesis," have been virtually unchanged and have been used continuously since that time to present (called "Current"). Actuarial analysis shows survival rates at 10, 20, and 30 years for AVR were 53%, 23%, and 8%, respectively, and for MVR were 51%, 23%, and 8%, respectively; for AVR, the 40-year survival was 4%. The standard error for all these values was 1%. There have been no deaths from structural valve deterioration (SVD) among patients with the "current" valves. The survival and incidence of thromboembolism with "current" valve are shown in Figure 8 (60).
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Figure 8 (A) Actuarial survival curves after aortic valve regurgitation (AVR) and mitral valve regurgitation (MVR) in the "current" Starr-Edwards valves. (B) Kaplan-Meier (KM) actuarial and actual freedom from thromboembolism after AVR and MVR with "current" valve. From Gao et al. (60).
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High-temperature-fixed (HTF) bioprosthesis in the young.
From January 1991 to September 1998, 50 young patients (ages range 7 months to 35 years; 22.7 ± 6.8 years) underwent single HTF bioprostheses in two hospitals (Paris and Ho Chi Minh City) based on social, medical, and geographical contraindications to anticoagulants. At nine years the actuarial survival was 95 ± 3.6%, and freedom from reoperation was 87.6 ± 7.1% (61); 91.7 ± 8% after AVR and 80% ± 12.6 after MVR.
Comment
Does HTF represent another important aspect of bioprosthetic preparation? HTF at 30° to 50°C ("Thermo Fix") is used for preparation of the Edwards PERIMOUNT MAGNA valve.
SVD of St. Jude Toronto stentless porcine valve.
At 5 and 10 years, the actuarial survival rates were 89.2% and 68%, respectively, and the rates of actuarial freedom from SVD were 98.8% and 77.9%, respectively (62).
Comment
The rate of SVD at 10 years is similar to that seen with stented porcine valves (63).
Low rate of use of bioprostheses for AVR in patients 65 years?.
Eighty thousand four hundred seventy patients aged 65 years undergoing AVR during 1999 to 2001 were identified from 1,045 U.S. hospitals’ Medicare Part A files (64). Use of bioprostheses increased from 28% in the first decile to 68% in the10th decile of hospital volumes. Bioprosthetic valve use increased (p < 0.001) from 44% in 1999 to 52% in 2001, and with age, from 36% in patients aged 65 to 69 years and to 60% in patients age 90 years.
Comment
The only data from randomized trials showing the very low rate of SVD after bioprosthetic AVR in those age 65 years is from the Veterans Administration trial whose 18-year (mean 15 years) follow-up data was published in the Journal of the American College of Cardiology in October 2000 (65). Also see discussion of surgery in octogenarians in the preceding text. It would be of interest to have similar data for 2004 to 2005.
Homograft replacement of the mitral valve.
The operative mortality in 108 patients was 3.8%. The estimate ("actual") of reoperation was 19% at eight years; 80% of reoperations were due to SVD (66). At eight years, the survival was 80 ± 6%; freedom from cardiac events (cardiac deaths and reoperation) was 71 ± 6%. There were 5 reoperations within 3 months and 10 late reoperations.
Operative mortality for replacing mitral PHV.
Operative mortality was 4.7% (5 of 106 patients) (67). Multivariate analysis showed prior myocardial infarction and "non-elective" surgical status were statistically significant predictors of mortality.
Hemodynamic performance of various PHVs.
Carpentier-Edwards pericardial (CEP; PERIMOUNT) versus Medtronic Mosaic (MM) Porcine (MMP). 1) An in vitro study of transvalvular resistance versus flow rate of <2 to >7 l/min in valve sizes 21, 23, and 25 MMP had lower resistance than the CEP at low flow rates (3 l/min), after which the MMP showed steep increases in resistance, and at flow rates of 4 l/min the CEP had much lower rates of resistance (Fig. 9) (68). 2) A prospective randomized trial of 100 patients. Prosthetic heart valve areas of the Perimount were larger than those of MMP in the 23 and 25 aortic annulus diameter (71) (Table 4).
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Figure 9 An in vitro study of transvalvular resistance versus flow rate of <2 to 7 l/min in valve sizes 21, 23, and 25 Medtronic Mosaic Porcine valve (MM) and Carpentier Edwards Pericardial (Perimount valves) (EP). Adapted from Kuehnel et al. (68). Cardiac index in two studies of normal humans was 3.6 ± 0.9 (SD) l/min/m2. Translating that to cardiac output in (l/min) in humans with small, moderate, or large size body surface areas (body surface areas [BSAs] of 1.5, 1.75, and 2.0 cm2) shows the normal cardiac outputs range from 4.1 to 9.0 l/min. At these flow rates (shaded areas) the Carpentier Edwards Pericardial clearly offers much lower resistance. Cardiac indexes in normals are from Barratt-Boyes and Wood (69) and Ehsani et al. (70). It is important that in vitro studies of prostetic heart valve evaluate flow rates that are appropriate for normals.
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A comparison of four supra-annular bioprosthesis in patients with small aortic annulus. A comparison of the CE Pericardial (Magna) to the CE Pericardial (Perimount), MMP, and Soprano valves in the 18- to 20-mm annulus diameter showed there was no statistically significant difference in valve areas. In the 21- to 23-mm annulus diameter the CE-Magna had the best hemodynamics (72) (Table 5).
Hemodynamic performance of other PHVs.
Nineteen-mm MMP has a high incidence of mismatch:
In 81 consecutive patients (69 female), mean age 78.0 ± 4.6% moderate valve prosthesis-patient mismatch (VP-PM) (defined as valve areas >0.65 to 0.8 cm2/m2) occurred in 49.4% and severe VP-PM (valve areas 0.65 cm2/m2) occurred in 50.6% (73). The 30-day mortality was 9.9%, and survival at 1 and 2 years was 78.5 ± 4.6% and 69.1 ± 5.5%, respectively.
Bileaflet mechanical PHVs valve sizes in 21-mm valve holder. In an in vitro model, at flow rates of >4 l/min, the St. Jude Medical Regent-19 and the Sorin Bicarbon Slim line had larger effective valve orifice areas than the ATS 18-mm, On-X 19-mm and Carbomedics Top Hat (<0.005) (74).
Valve prosthesis-patient mismatch.
Effect of MVR on PA hypertension: Of 56 patients with "normally" functioning mitral PHV (75), 30 patients (54%) had PA hypertension, defined as systolic PA pressure >40 mm Hg, and 40 patients (71%) had VP-PM, defined as prosthetic MVA 1.2 cm2/m2. There was a "significant" correlation (r = 0.64) between systolic PA pressure and prosthetic MVA. The systolic PA pressure in those with VP-PM was significantly higher than in those without VP-PM, 46 ± 8 mm Hg versus 34 ± 8 mm Hg (p < 0.001). In multivariate analysis, prosthetic MVA was the strongest predictor of systolic PA pressure. The authors concluded that persistent PA hypertension is frequent after MVR and is strongly associated with the presence of VP-PM.
Comment
The accompanying editorial describes some of the limitations of the study (76).
Moderate/severe VP-PM is associated with less LV mass regression. Patients with moderate/severe VP-PM (PHV area <0.9 cm2/m2) had less LV mass regression after AVR compared to those with mild VP-PM (PHV area 0.9 cm2/m2) 48 ± 47 g versus 77 ± 49 g (p = 0.002) (77). The other independent predictors of greater LV mass regression were female gender and higher preoperative LV mass.
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Footnotes
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Dr. Rahimtoola is a Distinguished Professor, University of Southern California; the George C. Griffith Professor of Cardiology; and a Professor of Medicine, Keck School of Medicine at USC. This review includes articles published from July 2004 to June 2005, with one exception. Dr. Rahimtoola has received honoraria from ATS; Edwards Life-Sciences; St. Jude Medical; Pfizer; American College of Physicians; the American College of Cardiology Foundation; Indiana University; the University of California, Los Angeles; the University of California, Irvine; Northwestern University; Cornell University; Creighton University; Thomas Jefferson University; Cedars-Sinai Medical Center; Harvard Medical School; and the University of Wisconsin.
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S. H. Rahimtoola
The Year in Valvular Heart Disease
J. Am. Coll. Cardiol.,
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S. H. Rahimtoola
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Heritable component of Valvular...
Atherosclerosis, calcification,...