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Physical Therapy for Heart Failure

Mechanisms of Improvement to Myocardial Perfusion after Exercise Training in Ischemic Cardiomyopathy
Romualdo Belardinelli
ULancisi Heart Institute, Ancona, Italy

Clinical Efficacy and Cost-Benefit Analysis of Nocturnal Home Oxygen Therapy in Patients with Chronic Heart Failure and Sleep-Disordered Breathing
Yoshihiko Seino
Nippon Medical School, Tokyo, Japan

Interventional Cardiology in the Elderly: Update of Non-Surgical Interventions for the Treatment of Cardiac Failure in Valvular Disease
Alain Cribier
Charles Nicolle Hospital, University of Rouen, Rouen




Mechanisms of Improvement to Myocardial Perfusion after Exercise Training in Ischemic Cardiomyopathy

Romualdo Belardinelli
ULancisi Heart Institute, Ancona, Italy

 

Accumulating evidence shows that exercise may have therapeutic benefits in heart failure, beyond being a stressor useful for diagnostic purposes. An inverse correlation between the level of physical activity (the fitness level) and the level of events and survival was found in an analysis of 1000 normal patients in randomized trials. In short, survival was best in the persons who were more active.

Myers and colleagues reported that in 7,600 males with and without cardiovascular (CV) disease that the higher level of exercise capacity the lower the risk of death. A peak oxygen uptake above 30 was associated with a 5-fold less risk of death compared to a peak oxygen uptake less than 30, independent of the presence or absence of CV disease.

Factors predictive of improvement in functional capacity after exercise training (ET) in chronic heart failure patients (CHF) include a low peak VO2 (<14 mL/kg/min), an abnormal relaxation pattern of left ventricular (LV) diastolic filling, a normal cardiac output/workrate slope, hibernating “viable “ myocardium, BMI <30, and male sex. This suggests that with the presence of abnormalities in the heart and pulmonary circulation, there would be less chance to improve functional capacity in these patients. Thus, based on these studies, the periphery seems to be less important than these central factors.

 

Improved myocardial perfusion

Myocardial perfusion can be improved with 8-weeks of ET. Improvement in myocardial perfusion can translate into better survival. For example, in a patient with ischemic cardiomyopathy (ICM), before ET there was a clear abnormality in the ECG suggesting myocardial ischemia with stable angina, and at the end of the 8-week ET the ECG was normal, an improvement in myocardial scintigraphy. This was an intriguing observation.

The number of viable segments before ET was predictive of the functional capacity in patients exercised at 60% of peak oxygen uptake for 8-weeks, in a 1998 report by Belardinelli and colleagues. Functional capacity was improved after 8-weeks ET in the patients with improved contractility with a low-dose dobutamine stress echocardiography, improved LV ejection fraction (LVEF), and systolic wall thickness core index. Thus, identifying hibernating myocardium before ET may be predictive of improvement in functional capacity and myocardial perfusion in patients with ICM.

 

Oxidative stress and exercise

Exercise may be an important tool, but the type, intensity, and the modality of exercise must be considered. Physical exercise may determine oxidative stress, and a high level of oxidative stress is associated with endothelial dysfunction, which can result in a less marked improvement of functional capacity. A low or normal level of oxidative stress is associated with absent or mild endothelial dysfunction and greater improvement in functional capacity. For example, in a patient with hypercholesterolemia, after 30 minutes of acute exercise, in the high intensity group (80% of VO2 max) there was a paradoxical 25% reduction in the flow-mediated dilation of the brachial artery, while in the mild intensity group (40% VO2 max) there was a marked 90% improvement in flow-mediated dilation. These changes were correlated to oxidative stress, as measured by plasma malondealdehyde, which was markedly increased in the high intensity group (from about 30 to 50 nmol/mL) and not increased in the low intensity group (about 25 nmol/mL).

In another study, they tested the oxidative stress after eccentric exercise, known to be a greater stimulator of oxidative stress, and found that in patients with ICM the increase in plasma malondealdehyde was earlier after eccentric exercise compared to in healthy subjects.

But, exercise may also induce important adaptation in the heart and vessel. Genes coding anti-oxidant enzymes are over-expressed by a program of ET in patients with CHF. Researchers from France showed that the gene of nitric oxide synthase and superoxide dysmutase is increased by ET, suggesting that an improvement in endothelial function may play an important role.

Brown and colleagues showed that when looking at coronary internal dimensions and flow resistance during isometric exercise, with handgrip there was a 10% reduction in the luminal area. In the presence of coronary stenosis this can cause myocardial ischemia. But for handgrip plus nitroglycerin, there was dilation of the coronary artery (about 30% increase in luminal area), which was about the same level with sublingual nitroglycerin. So, this is an important concept to consider when exercising patients with coronary stenosis.

Nitric oxide was found to be involved in this reaction. Gordon and colleagues showed that during aerobic exercise in the presence of coronary artery stenosis there is a tendency towards a constriction of the segments with mild stenosis or more severe stenosis, which behaves as it would after administration of acetylcholine. Importantly, post-exercise constriction is likely related to a lack of nitric oxide. After atrial pacing, normal coronary artery segments dilate, but pre-stenotic and stenotic vessels are narrowed, meaning myocardial perfusion may be deteriorated in those segments.

So, different problems are present. Exercise and myocardial perfusion in the coronary vessels is related to the presence or absence of abnormalities in the vessels. The abnormalities may be anatomical (stenosis), functional (vasomotor tone, endothelial dysfunction, autonomic imbalance) or both. The myocardium may be normal, or coupled with varying amounts of abnormal myocardium (necrotic, stunned, hibernating, fibrotic). These may be 4 models that may be seen frequently in clinical practice. For example, a patient may have single vessel disease with stunned myocardium, or multiple vessel disease with stunned myocardium, or single vessel disease with necrotic area and hibernating myocardium, or multiple vessel disease with necrotic area and hibernating stunned myocardium. This may affect the response to ET. 

Work by White and colleagues reported in 1993 showed that after ameroid occlusion of the left circumflex in the porcine model that 4 weeks of ET was associated with an astonishing increase of the vascularity of the coronary tree, especially the small vessels, compared to the control animal. This suggests sort of an angiogenesis or arteriogenesis can be stimulated by exercise.

In a human model, after gated SPECT and ET (60% of peak VO2, 3 times per week, 6 months) there was a dramatic reduction in the perfusion defect in the septal inferior wall with nearly complete reversibility.

 

Hypothesis One

There are several hypotheses that may explain the improvement of myocardial perfusion in this human model of ICM. One hypothesis may be coronary stenosis regression with ET. Hambrecht and colleagues showed that after a program of aerobic exercise there was no disease progression in the majority of patients, and regression in a minority of patients, indicating that with ET it is possible to obtain a sort of stabilization of the plaque and possibly an improvement in myocardial perfusion.

In the SCRIP study in 300 patients followed for 4 years, coronary artery disease (CAD) progression was reduced by 47% in the multifactorial risk reduction group, compared to the usual care group. The hospital readmission rate was 76% in the usual care group. In the multifactorial risk reduction group, triglycerides were reduced 20%, total cholesterol 40%, and LDL cholesterol 23.5%, and HDL cholesterol increased 12% and exercise capacity 20%. There was no change in the parameters in the usual care group. This suggests that a reduction in the progression of CAD or regression of CAD may be a possible explanation.

A study by Belardinelli and colleagues in patients after PTCA, showed that a 6-month ET program was associated with a reduction in total cholesterol, smoking, and triglycerides and an improvement in BMI. In the untrained patients, a 25% progression of CAD was found, compared to a 7.6% progression in the trained patients. No change was found in 89% of the trained patients and 75% of the untrained patients. A 4.4% regression of CAD was found in the trained patients, compared to no regression in the untrained patients.

 

Hypothesis Two

The second hypothesis is vascular remodeling. The vascular tree attempts to compensate for problems in perfusion and is able to react to different stimuli, for example shear stress or increasing metabolic demand in ischemic tissue by remodeling. This can lead to more direct blood flow. In one example, after 6-months of ET, an improvement in myocardial perfusion and extension of the defect is reduced by 30%, with remodeling of the vessel. This also translated into an improvement in LV function, with EF increasing from 42% to 49% at the end of the study. Clear improvement in contractility was seen.        

 

Hypothesis Three

Belardinelli and colleagues demonstrated that an improvement in myocardial coronary collateralization after ET in a model of ICM determines an improvement in myocardial perfusion. Improvement in contractility was associated with an improvement in myocardial perfusion, which was not due to just a peripheral effect of ET, as shown by the improved systolic blood pressure and systolic volume inverse relation in the trained patients versus controls.

Myocardial blood flow is increased in the collateral-dependent region in part because of an endothelium-dependent mechanism. This may be evident when the extent of the infarction is below 50% of the heart. They found that after ameroid plus 8-week ET, the number of the small vessels increased. This may be related to a mechanism of ateriogenesis. In fact, in dogs treated with FGF and VEGF, they found improved collateral-dependent blood flow after acute myocardial infarction, which was in part related to nitric oxide.

Several angiogenic peptides can be involved in this regulation. These peptides may be different on the basis of severe coronary artery stenosis. An endothelium-independent mechanism also plays a role. Work by Symons and colleagues showed that dipyradimole increases the concentration of adenosine in the myocardium, and there is an increase in the transmural coronary blood flow that is not very different than that obtained from with diltiazem, an endothelium-independent dilator. In a study by Belardinelli and colleagues, dipyradimole plus ET resulted in an additive effect in patients with ICM, with a greater increase in the coronary collateral score than in patients treated with dipyradimole alone. These changes were also associated with improvement in myocardial perfusion that was more marked in dipyridamole plus ET compared to dipyradimole alone. Systolic wall thickness core index was less marked. Improvement in the collaterals was found that was more evident in the dipyridamole plus ET group.

Arteriogensis and angiogenesis may be involved in the same mechanism after ET. Ateriogenesis is defined as the enlargement of pre-existing collateral arterioles allowing increased blood flow to downstream tissue. Angiogenesis is defined as the proliferation of capillaries within tissue. The stimuli for ateriogenesis are increased shear stress, while for angiogenesis it is hypoxia/ischemia.

In the model of human ICM studied by Belardinelli, both ateriogenesis and angiogenesis probably contributed to an improvement in myocardial perfusion in the tissue. The mediators for arteriogenesis are MCP-1, TGF-beta, beta-FGF, PIGF, PDGF, and MMPs, and for angiogenesis they are TGF-alpha, alpha-FGF, beta-FGF, PIGF, PDGF, and MMPs. The result of ateriogenesis is remodeling of aterioles into collateral vessels, and of angiogenesis is formation of new capillaries.         

 

Hypothesis Four

Endothelium-dependent dilation is a mechanism that has been postulated and demonstrated recently. ET may induce the expression of genes such as nitric oxide synthase, and may reduce the inactivation of nitric oxide. These are mechanisms that can contribute to the increase of the biological activity of nitric oxide. Hambrecht and colleagues demonstrated that 1-month of ET improved the vasomotor response and endothelium-dependent response in the treated coronary artery. Sessa and colleagues demonstrated an increase in ecNOS expression in animals.

In animals, an increase in myocardial capillary diffusion capacity after ET has been shown by Laughlin and colleagues. This likely explained the improvement in myocardial perfusion in the canine model.

Continued ET is associated with continued improvement in patients, as shown by Belardinelli and colleagues. The improvement achieved after 8-week of ET was maintained at 1 year. Sustaining an improvement in myocardial perfusion is likely to improve prognosis. Data from the ETICA study by this group, published in 1999, showed that improved myocardial perfusion is associated with an improved prognosis. After coronary angioplasty, in the training group after 6-months of ET at 60% of peak VO2, total myocardial perfusion was improved, which was associated with an improvement in peripheral endothelial function. Continued ET in these patients showed progressive improvement over a 6-year period. Importantly, this means it would be possible to sustain the improved perfusion. Improved myocardial perfusion over time is predictive of a better prognosis.

 

Conclusion

Chronic exercise may induce structural and functional adaptation in the coronary vessels that can determine an improvement in myocardial perfusion. Several mechanisms may be involved. ET may exert a direct action or an indirect action. The direct action is mediated by an increase in shear stress that determines a cascade of events, and determining an improvement in vasomotor function. Indirect action is related to an improvement of the coronary risk profile, especially in patients with ICM, determining a reduction in arteriosclerosis progression. The field of exercise-induced improvement in myocardial perfusion is very intriguing, but a definitive conclusion in this field has not been achieved yet.

 

 

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Clinical Efficacy and Cost-Benefit Analysis of Nocturnal Home Oxygen Therapy in Patients with Chronic Heart Failure and Sleep-Disordered Breathing

Yoshihiko Seino
Nippon Medical School, Tokyo, Japan

 

Evidence that sleep apnea, described as Cheyne-Strokes respiration, may adversely affect the pathophysiology and outcomes of chronic heart failure (CHF) is increasing. Sleep apnea has been suggested as the next therapeutic target in CHF.

Sleep-disordered breathing (SDB) comprises 2 major forms in CHF. Obstructive sleep apnea results from sleep-induced episodes of partial or complete upper airway collapse. The risk factors for obstructive sleep apnea differ by gender; an increase in BMI or obesity in men and age in women. Central sleep apnea arises from the lack of neuronal impulse to respiratory muscles. The principle risk factors for central sleep apnea are male sex, increasing age, hypercapnia, and atrial fibrillation, but not obesity.

 

Cheyne-Stokes respiration

A prevalence of 33% to 55% for central sleep apnea has been reported in the 3 major studies in patients with CHF.  Enhanced sensitivity of the ventilatory response to carbon dioxide in patients with CHF with central apnea was reported by Javaheri and colleagues. Enhanced sensitivity to carbon dioxide destabilizes breathing during sleep, making this an important pathological factor in CHF. 

During sleep, PaCO2 rises and becomes the most potent stimulus for augmented breathing. When the PaCO2 falls below the apneic threshold, driven by the hyperventilation, sleep apnea follows. Apnea persists until PaCO2 rises above the threshold required to stimulate the ventilatory response. The result is periodic breathing with recurring cycles of apnea and hyperventilation, namely, Cheyne-Stokes respiration.

Once triggered, the pattern of alternating hyperventilation and apnea is sustained by a combination of increased ventilatory chemoreceptor drive, pulmonary congestion, and apnea-induced hypoxia, which causes oscillation in PaCO2 above and below the apneic threshold. Central sleep apnea elicits chemical, neurohormonal, and hemodynamic oscillations including apnea, hypoxia, and oscillation in PaCO2, which provokes periodic elevation in the sympathetic nervous system, and surges in blood pressure and heart rate.

Lanfranchi and colleagues presented the prognostic value of the Cheyne-Stokes respiration in patients with NYHA class II-III heart failure. Multivariate analysis revealed that the apnea hyperpulmonary index (AHI) and left atrial size were the only independent predictors of subsequent cardiac death.

Although nocturnal oxygenation therapy using continuous positive air pressure (CPAP) has been employed recently for the treatment of sleep apnea, the effects of more convenient nocturnal home oxygen therapy (HOT) in patients with CHF and central apnea has not been verified.

 

Study design


Figure 1. Specific Activity Scale Questionnaire.
Click to enlarge

Thus, this group conducted a multi-center, open-label, randomized control trial to evaluate the efficacy of nocturnal HOT on SDB, oxygenation saturation, cardiac function, neurohormonal factors, and quality of life (QoL) assessed by the Specific Activity Scale in patients with CHF and central sleep apnea. The cost-benefit analysis was a substudy.

To assess the Specific Activity Scale (SAS), patients were asked to specify whether or not the patient could perform each type of activity without symptomatic limitation, according to the SAS scale questionnaire (Figure 1). Summarizing the questionnaire data, a given number of metabolic cost (METs) was derived for each patient for the self-perceived exercise tolerance.

The inclusion criteria for this study were stable outpatients over 20 years of age, NYHA class II-III, oxygen desaturation index (ODI) þ 5 dips/hour, and a left ventricular ejection fraction (LVEF) <45%. The control group received conventional therapy and the HOT group received conventional therapy plus nocturnal HOT via nasal cannulae (3 l/min) using an oxygen concentrator. Follow-up was 12 weeks. Patients with predominant obstructive sleep apnea were strictly excluded from the study.

 

Study results


Figure 2. Baseline characteristics in the study patients.
Click to enlarge

Figure 3. Polygraphical recordings in a representative patient before therapy nocturnal home oxygen therapy.
Click to enlarge

Figure 4. Polygraphical recordings by in a representative patient after nocturnal home oxygen therapy.
Click to enlarge

The baseline characteristics are shown in Figure 2. A total of 68 patients were enrolled from 20 centers and 56 patients were randomly assigned to the 2 groups. There were no significant differences in the baseline characteristics between the groups, with respect to age, gender, sex distribution, underlying heart disease, NYHA class, Specific Activity Scale, medications, ODI or AHI.

In a representative patient, a 43-year-old male with a 26% LVEF, NYHA class III heart failure, a BNP level of 1280 pg/ml, and a 2.5 Mets SAS (Figure 3), Cheyne-Stokes respiration completely disappeared, associated with stabilization of arterial oxygen concentration, after 12 weeks of nocturnal HOT therapy (Figure 4). Further, the NYHA class improved to class II moderate, BNP decreased to 1070 pg/ml, SAS increased to 5.5 METs, and peak VO2 increased to 14.7 ml/kg/min. 

Nocturnal HOT for 12 weeks, significantly improved overnight arterial ODI from 9.5 dips/hour to 5.9 dips/hour, and the AHI was reduced from 21 to 10 events per hour, indicating stabilization of Cheyne-Stokes respiration. In the control group, there was no significant change during the study period.

The initial values of the SAS were nearly identical in the 2 groups. Over the 12 weeks, a progressive increase in the SAS score was seen in the nocturnal HOT group, while it remained the same in the control group. The between group difference was significant at 12 weeks, indicating that HOT improved QoL, as assessed by SAS.

Plasma ANP, BNP, and norepinephrine concentrations, obtained every 4 weeks in the early morning, were unchanged by 12 weeks of HOT therapy. No significant change in PaCO2 was found. A significant improvement in LVEF was found in the HOT group, while there was no change in the control group (p=0.022). In summary, the results of the main study showed that nocturnal HOT stabilized Cheyne-Stokes respiration and arterial oxygen. These improvements were associated with improvement in cardiac function, LVEF, and QoL.

 

Cost-benefit analysis

The cost of illness was analyzed based on a questionnaire survey of the morbidity in patients receiving nocturnal HOT for more than a 6-month period, including the study period. The reduction in cost of illness following nocturnal HOT per year per patient was defined as a benefit from treatment. The charge for the nocturnal HOT was defined as a cost.

The survey questionnaire was sent to 33 physicians at 20 institutions who participated in the present nocturnal HOT study. The questionnaire asked about frequency of hospitalization, emergency room visits, and routine outpatient visits. The return rate for the surveys was 85.3% and the data was collected regarding 53 patients.

After nocturnal HOT, the incidence of hospitalization was remarkably reduced from 2.1 to 0.5 times per year, a 76% reduction. The routine outpatient visits were slightly reduced from 17.7 to 12.6 visits per year. The emergency room visits were markedly reduced from 2.5 to 0.7 visits per year, a 72% reduction.

Medical costs were estimated using the database of the central health insurance association in the Ministry of Health and Welfare (February 2003). The DPC MDC 5 diagnosis procedure combination charge for the hospitalization due to heart failure was applied, and the standard model case estimation for the emergency room visit or routine outpatient visit.

Nocturnal HOT therapy was associated with a reduction of 2 million yen in the cost of hospitalization over 1 year, a reduction of 15,000 yen in the cost of emergency room visits over 1 year, and a reduction of 6,000 yen in routine outpatient visits over 1 year. The cost/benefit per year was associated with a total savings of 1,298,390 yen, including the cost of the nocturnal HOT.

Because the cost of hospitalization is a major component of the cost of treating CHF, a sensitivity analysis based on the length of hospitalization was added. The same database was used, which defined the average hospital length of stay for uncomplicated heart failure as 33 days for DPC MDC 5. The sensitivity analysis revealed that a cost reduction with nocturnal HOT is expected for hospitalization exceeding 16 days.

 

Conclusion

The present study demonstrated the clinical efficacy and remarkable cost/benefit of nocturnal home oxygen therapy as a novel non-pharmacologic treatment for patients with CHF and central sleep apnea. The algorithm for the treatment of the central sleep apnea-hypopnea syndrome in heart failure should include maximizing pharmaceutical therapy. In the setting of persistent SDB, HOT or CPAP therapy should be considered or medications such as theophylline or benzodiazepines. Heart transplantation may be required in appropriate candidates.     

 

 

 

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Interventional Cardiology in the Elderly: Update of Non-Surgical Interventions for the Treatment of Cardiac Failure in Valvular Disease

Alain Cribier
Charles Nicolle Hospital, University of Rouen, Rouen

 

Non-surgical interventional procedures offer new therapeutic solutions to patients, mainly elderly, for whom thoracic surgery is either declined or deemed to be of high risk, because of fragility due to age and comorbidities. Although the current gold standard is thoracic surgery for either valvular repair or replacement, today interventional cardiology plays an important role for treating mitral valve disease and mainly aortic stenosis.

 

Treatment of mitral stenosis

The metallic commissurotome is an instrument developed by Cribier and colleagues about 8 years ago, as an alternative to the treatment of mitral stenosis using an Inoue balloon. The high cost of the Inoue balloon technique is a problem in developing countries, especially where there is a very high incidence of mitral stenosis. Also, the Inoue balloon can create some mitral regurgitation and some complication in patients with valves that are very fibrotic and calcific.

The Inoue balloon is inflated in the center of the valve and the commissure of the valve is opened by traction. An alternative technique, mainly used in the United States, is the double balloon technique, which is more efficient to open the 2 commissures with a direct effect. The metallic valulotome designed by Cribier and colleagues has 2 metallic bars that selectively open the valvular commissure. The efficiency of the instrument to open very stiff, calcific, and fibrotic valves is much higher. Double commissural splitting is achieved in 86% of patients using the metallic valulotome technique, compared to only about 30% with the Inoue balloon.

The detachable metallic head of the metallic valulotome can be removed and reused up to 50 times, significantly reducing the cost of the procedure. The commissurotome is opened using hand-held pliers, up to a maximum of 40 mm. The instrument is introduced trans-septally, positioned in the middle of the valve, opened with the hand-held pliers multiple times, with excellent results. For example, the mitral valve area was increased from 0.95 cm2 to 2.07 cm2 in one patient.

A review of difficult cases in elderly patients with very calcific valves showed that percutaneous metallic commissurotomy was very successful. Overall, in their experience, in young patients the achieved MVA was 2.34 cm2, and in elderly patients with calcific valves the MVA was 1.67 cm2, exactly the same as achieved with the Inoue balloon in a good population.

In their more than 4 years of experience in more than 20,000 treated patients, they have demonstrated the efficacy of the metallic commissurotome, that complications are rare, and that there can be a major economic impact.

 

Endovascular repair of mitral insufficiency

Mitral insufficiency is regularly treated by surgical valve repair or replacement. Interventional cardiologists have tried to develop some programs where mitral valve repair could be done without the surgeon. This is futuristic and the research programs are ongoing.

The percutaneous technique evaluated to treat mitral regurgitation is a simulation of the Alfieri’s surgical technique, which consists of stitching the free edges of the mitral valve to create a double-outlet on the mitral valve and reducing the mitral regurgitation with 1 central stitch on the mitral leaflets. More than 600 procedures have been reported since 1990.

For endovascular repair, interventional cardiologists would like to use trans-septal access catheterization, perforating the septum, catching the mitral valve, and either stitching the valve or clipping the valve using a special tool. In animal experiments, results have been achieved that are exactly similar to that achieved with the Alfieri’s surgical technique. An alternative technique uses a nitinol clip (E valve) that catches the 2 leaflets; the catheter is introduced trans-septally.

Endovascular mitral repair using the coronary sinus is also being researched. This involves using the location of the coronary sinus in humans that is just around the mitral orifice. The investigators imagine the possibility of introducing inside the coronary sinus a retractable annulus adjusted to remodel the coronary sinus by narrowing the mitral valve annulus to improve the coaptation of mitral valve leaflets. In one experience, in 7 sheep, a 12 Fr sheath was introduced via the jugular vein, and resulted in an annulus diameter reduced from 2.55 cm to 1.83 cm (p=0.004). At 6 months, there was a patent coronary sinus, patent left circumflex, and no mitral regurgitation. It will be some years before this can be performed in patients.

 

Percutaneous treatment of aortic stenosis

 In elderly patients, the main concern is degenerative calcific aortic stenosis. The best treatment for aortic stenosis is aortic valve replacement, which is safe even in old patients and can be done in the majority of patients. However, many patients cannot undergo surgery, especially patients with very old age or comorbidities. Thus, balloon valvuloplasty and then aortic valve replacement were developed.

Balloon aortic valvuloplasty is still performed in many countries, and its use is increasing because of the aging of the population. Despite the fact that it is a palliative procedure, it can be re-done several times and prolong the life of the patient by 5 to 6 years. The technique today is much simpler, carries a low risk, and is much more efficient. Also, today the limits of balloon valvuloplasty are known, which are the usual persistence of significant stenosis, and the limit of increasing the aortic valve area above 0.8 cm2. So, the patients are left with some aortic stenosis. The high mid-term restenosis rate, which is unpredictable, can reach 80% at 1 year. However, the functional status of the patient may be improved after 1 year, despite the restenosis. Yet, all patients are told the procedure will have to be done again on average after 1.5 years.

The principle of balloon aortic valvuloplasty is to break the calcium in the very calcific valves by balloon inflation. The indications for balloon aortic valvuloplasty are elderly patients (mean age 84 years), with a very high surgical risk due to severely depressed left ventricular (LV) function or comorbidities, patients with major myocardial dysfunction (including cardiogenic shock) as an attempt to improve LV function before valve replacement (bridge to surgery), patients who need urgent surgery for noncardiac reasons, and repeat balloon aortic valvuloplasty for symptomatic restenosis (up to 4-5 times).

In their experience in 148 consecutive patients over 84years of age, death occurred in 4 patients (mainly in patients with cardiogenic shock or very poor LV function), stroke in 3 patients, ventricular fibrillation in 1 patient, persistent atrioventricular block in 2 patients, and surgical femoral complications in 8 patients. The complication rate has been decreased recently using a newer device.

 

Percutaneous heart valve implantation

The goal was to develop a biologic valve mounted in a specific stent, which could be delivered percutaneously via standard catheter-based techniques, within the diseased aortic valve. The initial target population is patients with severe calcific aortic stenosis who are deemed inoperable or an unacceptable risk for surgical valve replacement.

The last generation of the valve that is implanted in man comprises a tricuspid valve made of equine pericardium, which is sutured in a highly-resistant stainless stent, with a maximal diameter of 23 mm. It is delivered by inflating a balloon at 4 to 5 Atm, a regular pressure for balloon inflation, and it can be introduced with a 24 Fr sheath. The durability of this valve in bench testing is more than 5 years, satisfactory for the target population. The valve is crimped, using a crimper device, over a regular balloon, and introduced into a 24 Fr introducer without any resistance.

The valve can be implanted via the antegrade trans-septal approach or the retrograde approach via the femoral artery. In the antegrade trans-septal approach, a 24-Fr sheath is introduced inside the femoral vein, and the valve is introduced through the sheath. A long guidewire is introduced from the femoral vein and exiting from the femoral artery on the opposite side, providing excellent support for the valve implantation. The valve is positioned exactly where desired before inflation, in the medium part of the calcium deposits of the native valve leaflets. Accurate positioning is extremely important. The aim is to have a stent implanted at the exact site of the valvular calcification. During balloon inflation, the heart is stimulated at 220/min to block the flow and stabilize the balloon during inflation. A super-aortic angiogram is performed afterwards to observe the results. This procedure is performed local anesthesia, with a procedure duration of 90 minutes and 25 minutes of fluoroscopy time. In the retrograde approach, a minimum diameter of the femoral artery of 7 mm is required to introduce the 24 Fr catheter. The procedure is performed under local anesthesia, the duration is 60 minutes and fluoroscopy time 20 minutes.

Procedural results include a reduction to nearly zero in the mean gradient and a homogenous increase in the aortic valve area to 1.69 cm2.

 

Conclusion

Percutaneous interventions bring new and promising therapeutic alternatives for a large subset of patients with valvular disease and cardiac failure, who are too high risk or contraindicated for heavy thoracic surgery. The development of percutaneous valve implantation is particularly expected because of the increasing incidence of degenerative aortic stenosis in the aging population.

 

 

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