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Hemodynamics “Au Contraire” Despite Diastolic Flow Reversal
and Angiographically Severe Aortic Regurgitation
Aortic regurgitation (AR) is characterized by inadequate aortic valve closure that results in the reflux of blood from the aorta into the left ventricle (LV) during diastole. Assessment of the degree of regurgitation is paramount to clinical decision-making in patients with AR, because patients with severe AR most often require surgical intervention. Semiquantitative grading of AR with color and spectral Doppler echocardiography or with angiography is widely used, but both techniques are hindered by significant limitations. Furthermore, quantitative parameters such as regurgitant volume and fraction depend on loading conditions and can be reliably used only in certain scenarios.
One of the commonly used parameters is the pressure halftime (PHT), which measures the rate of equalization of pressure between the aorta and the LV. Its utility in the setting of AR has been validated. Intuitively, the longer the PHT is, the milder the regurgitation. However, PHT is a phenomenon dependent on multiple variables including blood pressure (BP), heart rate (HR), compliance of the receiving chamber, effects of vasopressors and the volume status of the patient. We report a case of unique hemodynamics in a critically ill patient with angiographically severe AR that we postulate was due to volume depletion and further confounded by elevated systemic vascular resistance (SVR).
Case Report. The patient is a 60-year-old white female with a history of atrial flutter (AF) and nonischemic biventricular heart failure with an ejection fraction (EF) of 25% (echocardiography a year and a half ago). This study also reported mild AR, moderate dilatation of the LV and moderate tricuspid regurgitation with blunting of the respirophasic changes of the inferior vena cava. She presented to an outside hospital with complaints of increasing shortness of breath and lower-extremity edema for 5 days and confusion for 2 days according to the history obtained from her family. The patient was alert upon admission, but did not seem coherent. Her vitals signs at the outside hospital included a blood pressure (BP) of 98/40 and a heart rate (HR) of 137. She was noted to be hypoxic with a room air saturation of 80% despite O2 therapy, and as a result, was sedated and intubated. The patient subsequently became hypotensive and required pressor support with a dopamine drip. Intravenous digoxin was given to decrease her HR, however, she remained tachycardic and hypotensive. She was subsequently transferred to our center. Prior to her transfer, she was on coumadin, furosemide, carvedilol and lisinopril as her only outpatient medications. All other history including social, family and review of symptoms was unobtainable, as the patient was on a ventilator.
On physical examination, the patient was afebrile, had a HR of 137, and a BP of 88/40 in both extremities. She was lying flat and intubated, but no jugular venous pulsations were appreciated. The carotid pulses were rapid with variable upstroke. Cardiovascular examination revealed variable heart sounds with no appreciable S3 or S4. Her HR was irregularly irregular. She was noted to have a 3/6 systolic flow murmur at the right upper sternal border. No diastolic murmurs or abnormal heart sounds were detected due to her tachycardia. Lung examination revealed a few crackles and transmitted sounds. Her peripheral pulses were +1 with cool extremities. No lower-extremity pitting edema was noted.
Her pertinent initial laboratory results included a hemoglobin/ hematocrit of 17/49; blood urea nitrogen/creatinine of 37/1.2, a troponin I of 4.1, brain natriuretic peptide (BNP) of 3,140 and arterial blood gas of 7.5/50/132/97%. All other laboratory values were within normal limits. Her chest X-ray was consistent with mild pulmonary edema and cardiomegaly. Initial electrocardiography (ECG) showed AF with variable conduction, a ventricular rate of 150 bpm and a left anterior fascicular block. An ECG from 6 months prior at an outside hospital showed atrial fibrillation with rapid ventricular response and left-axis deviation.
An echocardiogram was obtained initially, showing a severely reduced EF of 20% at a HR of 149 bpm, and it was decided to repeat the study once the patient’s HR improved. The patient was started on an amiodarone infusion after a bolus and also on a phenylephrine drip for BP support. She was continually diuresed with a presumptive diagnosis of congestive heart failure given her elevated BNP. Her HR dropped down into the 60s and her systolic BP remained in the 90s. A repeat echocardiogram was performed a few hours later and showed mild AS with an aortic valve area of 1.5 cm2, a mean gradient of 16 mmHg and mild AR. The PHT was determined to be 653 msec (Figure 1). The color-flow jet appeared to be eccentric and directed toward the septum. Vena contracta, jet width or jet area, hence, could not be accurately assessed. The aortic root appeared mildly dilated, and the aortic valve appeared moderately thickened and calcified with a suggestion of bicuspid morphology. It is important to note that the study was technically difficult, as the critically ill patient was mechanically ventilated with suboptimal transthoracic windows and suprasternal views.
To better guide therapy, right-heart catheterization (RHC) and left-heart catheterization (LHC) were performed. The patient’s central aortic BP was 109/47 mmHg and her peripheral femoral BP was 134/53 mmHg (Figure 2). The HR was 62 bpm at the time of these procedures. The RHC numbers showed the following: RA 7 mmHg, RV 25/5 mmHg, PA 25/15 mmHg with a mean of 18 mmHg, and a PCWP of 10 mmHg (Figure 3). The patient’s cardiac output was 3.5 L/min with an index of 2 L/min/m2. Her pulmonary vascular resistance was 368 dynes sec/cm5 and her SVR was 1,531 dynes sec/cm5. The left ventricular end-diastolic pressure (LVEDP) did not show the steep rise commonly seen with severe AR and measured 7 mmHg (Figure 4). There was no significant gradient on pullback to suggest significant AS. LHC revealed a moderate stenosis in the distal left anterior descending artery. Coronary diastolic flow reversal was noted (Movie 1), with low aortic diastolic pressure, as well as a normal LVEDP, prompting the performance of aortography. The aortogram revealed 4+ AR (Movie 2) and dilation of the ascending aorta.
Cardiothoracic surgery was urgently consulted and the patient immediately underwent aortic valve replacement. Intraoperatively, the patient was found to have a bicuspid aortic valve with a dilated left ventricle. A #21 Edwards bovine pericardial prosthetic aortic valve was placed; a minimaze procedure, with removal of the left atrial appendage and plication of a sinus of Valsalva aneurysm, was also performed. The patient had a protracted postoperative course and was eventually transferred to a long-term rehabilitation center because of the inability to wean her off the ventilator. The patient’s dependence on ventilatory support was of unknown etiology, as a high-definition thoracic computed tomography scan and bronchoscopy revealed no obvious pathology.
PHT reflects the rate of equalization of aortic and LV diastolic pressures and is derived from AR jet continuous-wave tracings. With severe AR, there is rapid equilibration of the diastolic pressure gradient between the aorta and the LV, resulting in a shortened PHT. It can be derived from either echocardiographic Doppler or cardiac catheterization hemodynamic tracings. Regardless of the technique used, PHT correlates inversely with the angiographic severity (1+ = mild to 4+ = severe) of AR. Noninvasively measured PHT obtained from AR continuous-wave Doppler is considered a reliable and accurate method for evaluating the severity of AR.
Being a physiological variable, the rate of equilibration of aortic and LV pressures is dependent on a variety of hemodynamic factors. Factors that decrease LV compliance and/or increase LV filling pressure, such as LV hypertrophy secondary to HTN or concomitant AS and diastolic dysfunction, tend to decrease the PHT. Interestingly, tachycardia has the same effect. In this case report, we postulate that the presence of hypovolemia and the confounding effects of an elevated SVR led to a delay in the equalization of pressures between the aortic root and the LV. Furthermore, the filling pressures and/or compliance characteristics of the LV were such that severe (4+ on angiography) AR failed to increase the LVEDP steeply, as is characteristically seen in severe AR. During the second echocardiogram (obtained after the patient was diuresed aggressively), the patient’s BP was 124/53 (pulse pressure 71 mmHg) and her HR was 60 bpm. Based on an AR enddiastolic velocity of 3.5 m/sec, her end-diastolic pressure gradient between the aorta and LV was 49 mmHg and, hence, her LVEDP was 4 mmHg. PHT was now prolonged (653 msec), reflective of a low LVEDP, a lower HR and the effect of increased SVR. The LHC performed approximately 2 hours following the second echocardiogram correlated well with the calculated LVEDP from this same echocardiogram (LHC central aortic pressure 109/47, pulse pressure 62 mmHg, HR 62 bpm, LVEDP 7 mmHg), as illustrated in Figures 2 and 5. What was unusual, however, was the unexpected finding of angiographically severe AR on the aortogram (Movie 2).
Technical factors during an aortogram can sometimes spuriously cause significant AR. This is most commonly seen when catheters other than a pigtail catheter (PC) are used, or if the PC is positioned within or close to one of the aortic valve sinuses; significant AR occurs as a result of distortion of the aortic valve leaflet coaptation during forceful injections. This was, however, not the case in our patient in whom the PC was positioned appropriately in the ascending aorta away from the leaflets and 4+ AR was seen even on repeat aortography after repositioning of the PC. Thus, contrast angiography, being relatively independent of filling pressures, helped assess AR severity more optimally in this critically ill patient.
Discussion. To our knowledge, this is the first case reported that demonstrates mild AR by echocardiography with a falsely prolonged PHT and severe angiographic AR. This case illustrates unique hemodynamic findings not previously described in the literature. Therefore, we recommend that the rate of equilibrium between aortic and LV pressures should be interpreted in the context of real-time LV filling pressures as well as concomitant use of agents that increase SVR. We emphasize the importance of an integrated approach and the use of quantitative measures and, possibly, earlier utilization of an invasive modality in the evaluation of critically ill patients whenever practical.
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