History
In 1985 this previously healthy patient had a syncopal episode while driving. Presumably she was found to have high-degree atrioventricular block that was treated with implantation of a permanent dual-chamber pacemaker. Except for the diagnosis of moderate chronic obstructive pulmonary disease, the patient’s clinical course was uneventful until 2006, when she was hospitalized for acutely decompensated heart failure. During this hospitalization she underwent coronary angiography, which demonstrated the absence of coronary artery disease, and right heart catheterization, which demonstrated the following intracardiac pressures: right atrial, 18 mm Hg; pulmonary arterial, 88/34/53 mm Hg; and pulmonary artery wedge pressure, 25 mm Hg. Cardiac output was not measured, and hemodynamic response to vasodilators was not evaluated. Sildenafil was initiated at a twice daily dose of 50 mg.
Early in 2008 the patient required admission to the hospital for progressive exertional dyspnea, with more than 5 kg weight gain, increased jugular venous pressure, and anasarca. Admission weight was 117 kg, and renal function was severely compromised (blood urea nitrogen, 78 mg/dL; serum creatinine, 2.7 mg/dL). Transthoracic echocardiogram revealed mild left ventricular systolic dysfunction, mild-to-moderate mitral regurgitation into an enlarged left atrium, a markedly enlarged and hypokinetic right ventricle, severe tricuspid regurgitation into an enlarged right atrium, and an estimated pulmonary artery systolic pressure of greater than 65 mm Hg. To determine the appropriate therapy, hemodynamics were measured at baseline and after administration of excalating doses of inhaled nitric oxide (Table 5-1).
Based on these findings indicative of severe fluid overload, isolated venovenous ultrafiltration was initiated at a rate of 100 mL/hr and continued for 5 days. Weight and renal function changes observed with extracorporeal fluid removal were as shown in Table 5-2.
Before discharge the patient was placed on oxygen by nasal cannula at 2 L/min and on nightly bilevel positive airways pressure (BiPAP). The sildenafil dose was 20 mg three times daily, the endothelin receptor antagonist bosentan was initiated at a dose of 125 mg orally twice daily. At the follow-up office visit the patient reported improvement in exertional dyspnea and physical examination revealed a decrease in jugular venous pressure to 8 cm H2O, absence of pulmonary crackles, and minimal lower extremity edema.
The patient continued to improve until July 2009, when she reported increasing fatigue and was found to have atrial fibrillation. With the initiation of amiodarone, sinus rhythm was spontaneously restored. In March 2010, because of malfunction and generator battery depletion of the existing pacemaker, the patient underwent implantation of a dual-chamber permanent pacemaker and placement of two new right atrial and ventricular leads. Three months after implantation of the device, atrial fibrillation recurred, but at controlled ventricular rates of approximately 75 bpm, and sinus rhythm was restored with electrical cardioversion. Atrial fibrillation recurred in October 2010, and sinus rhythm was once again restored with electrical cardioversion. Yet another recurrence of atrial fibrillation was refractory to electrical cardioversion; over the subsequent 3 months, ventricular rates increased from 110 to 120 bpm. Over the ensuing weeks the patient experienced worsening exertional dyspnea and peripheral edema, which became increasingly more difficult to control despite frequent intensification of diuretic therapy. Early in December 2010 the patient underwent ablation of the atrioventricular node, which was associated with improvement in the signs and symptoms of congestion lasting until the end of 2011. Early in 2012 the patient began to experience worsening exertional dyspnea, weight gain, fatigue, and peripheral edema despite frequent adjustments of diuretic therapy.
TABLE 5-1
Hemodynamic Values at Baseline and after Administration of Inhaled Nitric Oxide
| Hemodynamics | Baseline | NO to 80 ppm |
| BP (mm Hg) | 93/61 | 71/46 |
| RA (mm Hg) | 21 | 18 |
| PA (mm Hg) | 71/26/45 | 63/21/42 |
| PAWP (mm Hg) | 12 | 16 |
| TPG (mm Hg) | 33 | 26 |
| CO (L/min), Fick | 5.2 | 6.1 |
| CI (L/min/m2), Fick | 2.5 | 2.9 |
| PVR (Wood units) | 6.4 | 4.3 |
| PVRI (Wood units/m2) | 13.2 | 9.0 |
BP, Arterial blood pressure; CI, Cardiac index; CO, cardiac output; NO, nitric oxide; PA, pulmonary arterial pressure; PPM, parts per million; PAWP, pulmonary artery wedge pressure; PVR, pulmonary vascular resistance; PVRI, pulmonary vascular resistance index; RA, right atrial pressure; TPG, transpulmonary gradient.
TABLE 5-2
Weight and Renal Function Changes Observed with Extracorporeal Fluid Removal
| Factors Measured | Day 1 | Day 2 | Day 3 | Day 4 | Day 5 |
| Weight (kg) | 117 | 114.5 | 112 | 109 | 104 |
| Blood urea nitrogen (mg/dL) | 78 | 60 | 45 | 40 | 34 |
| Serum creatinine (mg/dL) | 2.7 | 2.4 | 2.0 | 1.4 | 1.1 |
Comments
The patient had true pulmonary arterial hypertension as demonstrated by the coexistence of the three hemodynamic variables that define this disease entity: a mean pulmonary arterial pressure greater than 25 mm Hg at rest, pulmonary artery wedge pressure less than 15 mm Hg, and pulmonary vascular resistance greater than 3 Wood units. The cause of pulmonary arterial hypertension in this patient is unknown, but factors such as obesity, obstructive sleep apnea, and thyroid disease have been shown to contribute to its severity.8
Notably, after the first right heart catheterization, the phosphodiesterase inhibitor sildenafil was initiated without knowledge of the patient’s pulmonary vascular resistance or hemodynamic response to vasodilator administration. Practice guidelines recommend that drugs specific for pulmonary arterial hypertension be initiated only after a complete hemodynamic evaluation to avoid potentially deleterious effects in patients with pulmonary arterial hypertension secondary to left heart disease.8
In this patient, severe pulmonary arterial hypertension is the principal cause of right ventricular dysfunction manifested by the physical findings of venous congestion and peripheral edema, the elevated right atrial pressure, and echocardiographic evidence of right ventricular enlargement and decreased systolic function.8 Recent studies demonstrated that increased central venous pressure is a key determinant of worsening renal function because transmission of the elevated venous pressure to the renal veins further impairs the glomerular filtration rate by reducing net filtration pressure. On hospital admission the patient had severe renal impairment, which improved with extracorporeal fluid removal.1 Loop diuretics, the most commonly used medications to reduce congestion, block sodium chloride uptake in the macula densa, independent of any effect on sodium and water balance, thereby stimulating the renin-angiotensin-aldosterone system. This pathophysiology and the growing literature documenting the adverse consequences of diuretic use on acute heart failure outcomes has led to exploration of other approaches.1 Fluid removal by ultrafiltration at a rate that does not exceed the interstitial fluid mobilization rate of 14 to 15 mL/min avoids further activation of the renin-angiotensin-aldosterone system. Moreover, for the same fluid volume, more sodium is removed by isotonic ultrafiltration than by diuretic-induced hypotonic diuresis. In this patient, venovenous ultrafiltration was associated with a progressive reduction in weight and improvement in renal function.2
After approximately 12 months of clinical stability, the patient’s disease progression accelerated, as suggested by the increasing burden of atrial fibrillation. In addition, because the patient has right ventricular dysfunction, she tolerates rapid ventricular rates especially poorly. As in this patient, atrial fibrillation occurs in the majority of individuals in the setting of structural heart disease. Changes in metabolic, mechanical, neurohormonal, and inflammatory factors associated with heart failure contribute to the development of atrial fibrillation. However the mechanisms linking these factors to the development of the substrate for atrial fibrillation and its progression from paroxysmal to permanent are not completely understood. A recent Euro Heart Survey analysis documented that paroxysmal atrial fibrillation progressed to persistent forms in 178 of 1219 (15%) patients. On multivariable analysis, hypertension, age older than 75 years, previous transient ischemic attack, chronic obstructive pulmonary disease, and heart failure independently predicted progression of atrial fibrillation from paroxismal to persistent. Using the regression coefficient as a benchmark, the investigators developed a score to predict the risk for atrial fibrillation progression. Based on the presence of heart failure (2 points), history of chronic obstructive pulmonary disease (1 point), and age older than 75 years, the patient had a score of 4, indicative of moderate-to-high risk for progression from paroxysmal to persistent atrial fibrillation.3
The patient tolerates rapid ventricular rates poorly. This is typical of patients with right ventricular failure. In normal individuals, 85% of the blood volume is stored in the venous circulation and 15% in the arterial circulation. Patients with right ventricular failure have a larger proportion of the blood volume stored in the venovenous circulation, which renders them especially susceptible to intraarterial volume depletion. This risk is further accentuated if conditions such as atrial fibrillation with rapid ventricular response further compromise filling of the left ventricle.3
Current Medications
The patient’s current medications are torsemide 60 mg twice daily, hydrochlorothiazide 25 mg once daily 30 to 60 minutes before taking the torsemide, spironolactone 50 mg in the morning and 25 mg in the evening 30 to 60 minutes before taking the torsemide, potassium chloride 30 mEq daily, sildenafil 20 mg three times daily, bosentan 125 mg twice daily, warfarin 7.5 mg daily, aspirin 81 mg daily, levothyroxine 75 mcg daily, omeprazole 20 mg daily, and fluticasone-salmeterol 250/50 mcg, one inhalation twice daily.
Comments
The loop diuretic used in this patient is torsemide. It is preferred over furosemide because it has better oral bioavailability (unpredictable for furosemide, 100% for torsemide) and longer half-life (2.5 vs. 6.5 hours), which reduces the length of time of postdiuretic renal sodium retention. With chronic loop diuretic therapy the distal tubular cells adapt to reabsorb sodium more efficiently, thus reducing the natriuresis produced by loop diuretics. Because thiazide diuretics and aldosterone antagonists have a longer half-life than loop diuretics, the patient was instructed to take these medications before the loop diuretic to mitigate the effects of distal tubular adaptation to loop diuretics and thus maintain the effectiveness of torsemide.4
The patient’s therapy for pulmonary arterial hypertension included the phosphodiesterase inhibitor sildenafil and the nonselective endothelin antagonist bosentan. The presence of severe right ventricular failure warrants consideration of the addition of a prostacyclin preparation. This was not used in this patient because of concerns that this type of medication may increase intrapulmonary shunting when left ventricular systolic function is below normal and left cardiac filling pressures rise in response to inhaled nitric oxide.8
Therapy also did not include antiarrhythmic agents. The authors of the Euro Heart Survey analysis found that use of antiarrhythmic agents did not prevent progression of atrial fibrillation in high-risk patients and suggested that in these patients therapy should be aimed at controlling heart rate rather than rhythm.2 In this patient a rate control agent, such as diltiazem, was not used because its negative inotropic action could worsen the systolic function of the already compromised right ventricle and increase fluid retention.8
Current Symptoms
The patient’s current symptoms are dyspnea with minimal exertion, 5.4 kg weight gain, fatigue, increased oxygen requirements.
Comments
After ablation of the atrioventricular node the patient had a period of symptomatic improvement before experiencing the current clinical deterioration. This observation raises the question of which factor(s) produced the initial improvement and why such improvement was not sustained beyond 12 months. With right ventricular pressure overload, which in this patient’s case is due to pulmonary arterial hypertension, leftward bowing of the interventricular septum during diastole causes decreased left ventricular filling, chamber size, compliance, and contractility. Atrial fibrillation with rapid ventricular response further compromises left ventricular filling, thus increasing left cardiac filling pressure and decreasing forward cardiac output.9 This hemodynamic deterioration is the likely culprit of the worsening heart failure symptoms experienced by the patient. It is plausible that the clinical improvement occurring immediately after atrioventricular node ablation resulted from improvement in left ventricular filling permitted by slower heart rates.9
It is more difficult to explain why the clinical improvement occurring after atrioventricular node ablation persisted for almost 12 months. A recent study demonstrated that right ventricular pressure overload results in both myocardial and electrical remodeling.6 The effects of the latter—conduction slowing and action potential prolongation—contribute to the lengthening of right ventricular contraction duration and marked delay in right ventricular peak myocardial shortening and, consequently, in the onset of diastolic relaxation in contrast to the septum and the left ventricle.6 This interventricular mechanical dyssynchrony decreases left ventricular filling and stroke volume. Therefore left ventricular dysfunction, initially caused by left ventricular compression by the diastolic bowing of the septum, is maintained and amplified by low left ventricular preload and underfilling. It has been suggested that in patients with right ventricular pressure overload the interventricular delay in systolic contraction and diastolic relaxation may be improved with preexcitation of the right ventricle with right ventricular pacing.6 Therefore it is possible that the clinical improvement occurring in the patient after atrioventricular node ablation can be explained by the fact that, for a time, right ventricular pacing may have decreased diastolic interventricular delay and improved left ventricular filling and stroke volume.
After an extended period of relative clinical stability, the patient experienced a decline in functional capacity and worsening signs and symptoms of congestion. This clinical deterioration may be due to the detrimental effects of prolonged right ventricular apical pacing on cardiac structure and left ventricular function.10 This may be related to the abnormal electrical and mechanical activation pattern of the ventricles caused by right ventricular apical pacing. Several large, randomized clinical trials of pacing mode selection have suggested an association between a high percentage of right ventricular apical pacing and worse clinical outcomes. Pertinent to this case is the fact that the negative effects of apical right ventricular pacing may be more pronounced in patients with underlying conduction disease and those who underwent atrioventricular node ablation.10
Physical Examination
Comments
The patient’s physical examination findings are consistent with a “wet and cold” hemodynamic profile, in which a low cardiac output, suggested by a low systolic blood pressure, is associated with signs of fluid overload, manifested by an elevated jugular venous pressure, enlarged liver, and marked peripheral edema.
The right ventricular lift and the increased pulmonary component of the second heart sounds (S2) are consistent with marked right ventricular enlargement and dysfunction and with severe pulmonary arterial hypertension.8
Laboratory Data
Comments
The elevated blood urea nitrogen/creatinine ratio is a manifestation of the effects of an elevated central venous pressure on renal function. As explained earlier, an increase in central venous pressure produces a reduction in renal blood flow. The renal reabsorption of urea increases with decreasing renal blood flow. Therefore in this patient the elevation of blood urea nitrogen is due to increased renal reabsorption of urea resulting from the decrease in renal blood flow produced by the elevated central venous pressure.1
The patient’s serum potassium level is in the upper limits of normal as a result of the use of the potassium-sparing diuretic spironolactone in a patient with significant renal dysfunction.
According to the Modified Diet in Renal Disease (MDRD) equation, the patient’s estimated glomerular filtration rate is 40 mL/min/1.73 m2, consistent with moderate reduction in renal function. North American and European practice guidelines for the treatment of heart failure in adults include specific recommendations for the monitoring, prevention, and treatment of hyperkalemia in patients receiving aldosterone antagonists.7
Electrocardiogram
Findings
A 12-lead electrocardiogaram was obtained in November 2010, shortly before the patient underwent atrioventricular node ablation (Figure 5-1). The tracing showed atrial fibrillation with a ventricular rate of approximately 115 bpm. In addition, a leftward axis, right bundle branch block, and nonspecific T waves changes in the inferior leads were noted.
FIGURE 5-1
Comments
Atrial fibrillation with rapid ventricular response was associated with hemodynamic instability and worsening signs and symptoms of right ventricular failure because this arrhythmia further compromises left ventricular diastolic filling and aggravates venous congestion.
Some typical electrocardiographic features of pulmonary arterial hypertension are not seen in the patient’s tracing. Right atrial enlargement cannot be appreciated because of the presence of atrial fibrillation. Right axis deviation and right ventricular hypertrophy with a strain pattern also are absent.
Echocardiogram
Findings
The echocardiogram showed tricuspid annular systolic velocity before and after upgrade to cardiac resynchronization therapy (Figure 5-2, A), right ventricular area change before upgrade to cardiac resynchronization therapy (Figure 5-2, B), and right ventricular area change after upgrade to cardiac resynchronization therapy (Figure 5-2, C).
Comments
Right ventricular pressure overload is associated with negative left ventricular remodeling. On the other hand, left ventricular function greatly influences right ventricular systolic function. Left ventricular contraction is responsible for as much as 40% of right ventricular systolic pressure and cardiac output. In this patient the improved left ventricular performance resulting from cardiac resynchronization therapy appears to have increased right ventricular contractility, which, in turn, is associated with reduction in central venous pressure and in the signs and symptoms of right ventricular failure.
Computed Tomography
Findings
Noncontrast computed tomography of the chest at the level of the main pulmonary artery demonstrated markedly enlarged main, right, and left pulmonary arteries (Figure 5-3).
Comments
The computed tomography findings are consistent with the diagnosis of pulmonary arterial hypertension. Pulmonary arterial hypertension is characterized by intimal hypertrophy and fibrosis, smooth muscle hypertrophy, vasoconstriction, and adventitial proliferation with thrombosis in situ. These changes occur primarily in the small pulmonary arterioles and cause progressive dilation of the larger pulmonary vessels.
FIGURE 5-2 A to C.
FIGURE 5-3
Hemodynamics
Findings
Hemodynamic studies revealed systemic arterial hypotension, elevated right and left cardiac filling pressures, and severe pulmonary arterial hypertension (Table 5-3).
Comments
In contrast to the improvement obtained with optimization of pharmacologic treatment, the patient’s hemodynamic picture is now definitely worse. Noteworthy is the marked increase in pulmonary artery wedge pressure, which suggests progression of left ventricular dysfunction. The most plausible reason for this decrease in left ventricular performance is the detrimental effect of persistent apical right ventricular pacing on the electrical and mechanical activation pattern of the left ventricle.10
Focused Clinical Questions and Discussion Points
Question
Why did the patient’s atrial fibrillation progress from paroxysmal to persistent?
Discussion
The patient is at an increased risk for atrial fibrillation progression from paroxysmal to persistent because of her older age, underlying chronic obstructive pulmonary disease, and right heart failure. Although knowledge is increasing about the risk factors for atrial fibrillation progression, the specific electrophysiologic substrates favoring such evolution are incompletely understood. The scheme proposed by the Euro Heart Survey Investigators to predict atrial fibrillation progression bears a striking resemblance to the CHADS2 score used to predict thromboembolic events.3 Both reflect the advanced age of patients with atrial fibrillation and their high comorbidity burden, highlighting the fact that congestive heart failure, hypertension, previous stroke or transient ischemic attack, pulmonary disease, and diabetes are associated with a substrate favoring both the progression of atrial fibrillation and the development of complications associated with this arrhythmia.3 Another unresolved issue is the optimal treatment of paroxysmal atrial fibrillation at high risk for progression. Even less is known about selection of treatment for patients who develop atrial fibrillation in the setting of right heart failure caused by pulmonary arterial hypertension. The patient presented here was a poor candidate for both calcium channel blockers because of her severe right heart failure and congestion, and amiodarone, because of the fear that possible pulmonary complications may prove fatal in the setting of underlying pulmonary disease and severe pulmonary arterial hypertension. Although atrioventricular node ablation was the best option in this patient’s situation, it ultimately exposed her to the detrimental effects of continuous apical right ventricular pacing.10
TABLE 5-3
Comparison of Hemodynamic Monitoring Results before Atrial Fibrillation and before Upgrade to Cardiac Resynchronization Therapy
| Factors Measured | Before Onset of AF | Before Upgrade to CRT |
| BP (mm Hg) | 110/70 | 92/60 |
| RA (mm Hg) | 2 | 13 |
| PA (mm Hg) | 32/13/22 | 59/36/43 |
| PAWP (mm Hg) | 5 | 27 |
| TPG (mm Hg) | 17 | 16 |
| CO (L/min) | 3.8 | 4.1 |
| CI (L/min/m2) | 2.0 | 2.0 |
| PVR (Wood units) | 4.5 | 3.9 |
| PVRI (Wood units/m2) | 8.4 | 7.9 |
AF, Atrial fibrillation; BP, arterial blood pressure; CI, cardiac index; CO, cardiac output; CRT, cardiac resynchronization therapy, PA, pulmonary arterial pressure; PAWP, pulmonary artery wedge pressure: PVR, pulmonary vascular resistance; PVRI, pulmonary vascular resistance index; RA, right atrial pressure; TPG, transpulmonary gradient.
Question
Does pressure-induced right ventricular failure affect left ventricular function?
Discussion
It is known that right ventricular pressure overload leads to leftward bowing of the interventricular septum during diastole, thereby causing decreased left ventricular chamber size, compliance, and contractility. However, the impaired left ventricular function in this setting may not simply be the result of geometric effects of right vetricular enlargement and left ventricular chamber distortion. Electrophysiologic effects of right ventricular remodeling, such as conduction slowing and action potential prolongation, lengthen right ventricular contraction and delay the onset of diastolic relaxation with respect to the septum and the left ventricle.6 This interventricular dyssynchrony reduces left ventricular filling and stroke volume. In clinical observations and animal studies of pulmonary hypertension, ventricular interdependence was further manifested by left ventricular “atrophic” electrical and mechanical remodeling. Because interventricular delay in systolic contraction and diastolic relaxation occur in patients with right ventricular pressure overload, preexcitation of the right ventricle with right ventricular pacing may minimize diastolic interventricular delay and improve left ventricular filling and stroke volume.6 Attenuation of “atrophic” left ventricular remodeling by right ventricular pacing may explain the clinical and hemodynamic improvement experienced by the patient in the 12-month period between atrioventricular node ablation and recurrent clinical deterioration. Right ventricular outflow tract pacing, septal pacing, and bundle of His pacing have been proposed as alternatives to right ventricular apical pacing based on the hypothesis that closer proximity of the pacing site to the normal conduction system may result in less electrical activation delay and mechanical dyssyncrony.10 In this respect, however, not all studies have been uniformly positive. In a randomized study of 98 patients with atrioventricular block, no difference in left ventricular ejection fraction and exercise capacity occurred after 18 months of follow-up between patients treated with septal versus apical right ventricular pacing.10 In addition, in the patient described here, an alternative right ventricular pacing site would have probably been unattainable because of the difficulties in lead positioning and concerns about lead stability and threshold caused by the very large, pressure-overloaded right ventricle.
Question
Discussion
The negative effects of right ventricular apical pacing have been attributed to the abnormal electrical and mechanical activation pattern of the ventricles.5 During right ventricular apical pacing, the conduction of the electrical wavefront propagates through the myocardium, rather than through the His-Purkinje conduction system. As a result, the electrical wavefront progresses more slowly and induces heterogeneity in electrical activation of the myocardium, comparable to that of LBBB. Right ventricular apical pacing also changes the onset and pattern of mechanical activation of the left ventricle. In several animal studies the regions near the pacing site have rapid early systolic shortening, resulting in pre-stretch of the late-activated regions. Consequently, these regions have delayed systolic shortening, which imposes systolic stretch on the early activated regions undergoing premature relaxation. Redistribution of myocardial strain and work reduces the effectiveness of the subsequent contraction and produces changes in cardiac metabolism, perfusion, remodeling, hemodynamics, and mechanical function. Several studies have demonstrated the beneficial effects of the upgrade from right ventricular apical pacing to cardiac resynchronization therapy.10 These benefits include (1) reverse remodeling of the left ventricle, defined as a reduction in left ventricular volumes; (2) reduction in the severity of mitral regurgitation; (3) improvement in contractility, defined as an increase in dP/dtmax; (4) decrease in left ventricular end-diastolic pressure and isovolumic pressure half-time; (5) improvement in global left ventricular ejection fraction; and (6) improvement in exercise capacity and NYHA functional class.
However, it remains unclear whether upgrade to CRT in previously paced patients also improves survival.10 In the Post AV Nodal Ablation Evaluation (PAVE) trial, 184 patients were randomized after atrioventricular node ablation to conventional right ventricular pacing or cardiac resynchronization therapy. Mean left ventricular ejection fraction at follow-up was significantly lower in the 81 patients who underwent right ventricular pacing than in the 103 patients treated with cardiac resynchronization therapy (41 ± 13% vs. 46 ± 13%, p <0.05).5 Other trials have shown only modest differences in cardiac function and exercise capacity between patients treated with conventional right ventricular pacing and those receiving cardiac resynchronization therapy. The results of the BioPace (Biventricular Pacing for Atrioventricular Block to Prevent Cardiac Desynchronization) trial (NCT00187278) are not yet available.10
Of importance, no data are available on the effects of CRT in patients with features similar to those of the patient presented in this case study here—right ventricular failure resulting from severe pulmonary arterial hypertension and apical right ventricular pacing after atrioventricular node ablation.
Final Diagnosis
The patient’s final diagnosis was determined to be worsening biventricular systolic heart failure resulting from right ventricular apical pacing.
Plan of Action
The patient was referred to an electrophysiologist for consideration of device upgrade to a biventricular implantable cardioversion defibrillation device.
Intervention
In March 2012 the patient underwent removal of the generator of the existing pacemaker and insertion of a biventricular pacemaker.
Outcome
Shortly after upgrade from right ventricular to biventricular pacing the patient reported improvement in dyspnea and fatigue.
Findings
Physical examination revealed a blood pressure of 125/70 mm Hg, jugular venous pressure of 8 cm H2O, and trace pitting edema of the lower extremities. Hemodynamic measurements were repeated and compared to those obtained before upgrade from right ventricular to biventricular pacing.
Comments
The physical examination is consistent with improvement of congestion. Hemodynamic values indicate a reduction in right and left cardiac filling pressures and improvement in cardiac output (Table 5-4). These findings suggest that cardiac resynchronization therapy attenuates the detrimental effects of right ventricular apical pacing on left ventricular function and that improved left ventricular performance reduces the severity of right ventricular failure.10 This observation draws attention to the complex interactions between the two ventricles.9 As previously discussed, right ventricular pressure overload has profound detrimental effects on left ventricular electrical and mechanical remodeling.6,9 Conversely, left ventricular performance significantly affects right ventricular systolic function. Experimental studies have shown that approximately 20% to 40% of right ventricular systolic pressure and volume outflow result from left ventricular contraction.9 In this patient the improved left ventricular performance resulting from CRT may have enhanced right ventricular forward flow, which, in turn, is associated with a reduced central venous pressure and the signs and symptoms of right ventricular failure.10
TABLE 5-4
Hemodynamic Values with Right Ventricular Pacing and After Upgrade to Cardiac Resynchronization Therapy
| Factors Measured | RV Pacing | CRT |
| RA (mm Hg) | 13 | 9 |
| PA (mm Hg) | 59/36/43 | 39/14/22 |
| PAWP (mm Hg) | 27 | 7 |
| TPG (mm Hg) | 16 | 15 |
| CO (L/min) | 4.1 | 4.7 |
| CI (L/min/m2) | 2.0 | 2.3 |
| PVR (Wood units) | 3.9 | 3.2 |
| PVRI (Wood units/m2) | 7.9 | 6.5 |
CI, Cardiac index; CO, cardiac output; CRT, cardiac resynchronization therapy; PA, pulmonary arterial pressure; PAWP, pulmonary artery wedge pressure; PVR, pulmonary vascular resistance; PVRI, pulmonary vascular resistance index; RA, right atrial pressure; RV, right ventricular; TPG, transpulmonary gradient.
Selected References
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2. Costanzo M.R., Ronco C. Isolated ultrafiltration in heart failure patients. Curr Cardiol Rep. 2012;14:254–364.
3. de Vos C.B., Pisters R., Nieuwlaat R. et al. Progression from paroxysmal to persistent atrial fibrillation. J Am Coll Cardiol. 2010;55:725–731.
4. Dell’Italia L.J. Anatomy and physiology of the right ventricle. Cardiol Clin. 2012;30:167–187.
5. Doshi R.N., Daoud E.G., Fellows C. et al. Left ventricular-based pacing cardiac stimulation post AV nodal ablation evaluation (the PAVE study). J Cardiovasc Electrophysiol. 2005;16:1160–1165.
6. Hardziyenka M., Campian M.E., Verkerk A.O. et al. Electrophysiologic remodeling of the left ventricle in pressure overload-induced right ventricular failure. J Am Coll Cardiol. 2012;59:2193–2202.
7. Jessup M., Abraham W.T., Casey D.E. et al. 2009 Focused update: ACCF/AHA guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2009;119:1977–2016.
8. McLaughlin V.V., Davis M., Cornwell W. Pulmonary arterial hypertension. Curr Probl Cardiol. 2011;36:461–517.
9. Santamore W.P., Dell’Italia L.J. Ventricular interdependence: significant left ventricular contributions to right ventricular systolic function. Prog Cardiovasc Dis. 1998;40:289–308.
10. Tops L.F., Schlij M.J., Bax J.J. The effects of right ventricular apical pacing on ventricular function and dyssynchrony. J Am Coll Cardiol. 2009;54:764–776.
