relations between doppler tracings of pulmonary regurgitation and invasive hemodynamics in acute...

Relations Between Doppler tracings of Pulmonary Regurgitatdon and Invasive

Hemodynamics rn Acute Right Ventricular Infarction Complicating Inferior Wall

left Ventricular Infarction Ariel Cohen, MD, Philippe Guyon, MD, Christophe Chauvel, MD,

Eric Abergel, MD, Dominique Costagliola, PhD, Hanna Raffoul, MD, Jean Valty, MD, and Benoit Diebold, MD, PhD

To test the hypothesis that flow characteristics from pulmonary regurgitation (PR) can predict right ventricular

and the lowest mid-diastolic to peak early diastolic

(Rv) involvement in patients with inferior wall acute velocity ratio were significantly lower in group 1 than

myocardial infarction, we prospective tl

recorded con- in group 2 (91 f 31 vs 214 + 57 ms [p <0.0011,0.35

tinuous-wave Doppler tracings and rig t-sided cardiac 2 0.08 vs 0.59 f 0.13 [p =zO.OOll, respectively). The

hemodynamics in 48 consecutive patients with inferior best diagnostic accuracy (95%) was obtained with cutoff values of PHT

wall acute myocardial infarction and PR. Right heart hemodynamics enabled the identification of 29 patients

tolic to peak ea 4 5150 ms and the lowest mid-dias- diastolic velocity rotio ~0.5: sensi-

with (group 1) and 19 without (group 2) RV involve- My lOO%, specificity 89%, positive predictive value

ment. In patients with RV involvement, the ulmonary 94%, and negative predictive value 100%. Using mul-

regurgitant flow pattern was characterized Ii y a rapid tiple logistic regnzssion analysis, we found that PHT,

rise in flow velocity to a peak level followed by an was the strongest these parameters, s

redictor of RV involvement. Thus,

abrupt deceleration in mid-diastole, wherws in patients useful erived from pulmonary regurgitant

without RV involvement, the deceleration in mid-dias- tracings, are in the noninvosive bedside diagnosis of RV infarction.

tole was gradual. The pressure half-time of PR (PHT,,,) (Am J Cardiol 1995;75:425-430)

R ight ventricular (RV) infarction occurs almost exclu- sively in the setting of inferior wall left ventricular

myocardial infarction.*- 4 Its recognition is clinically important because patients with RV involvement are more prone to in-hospital morbidity and mortality than those with isolated inferior wall left ventricular myocardial infarction.5,6 Because of the limitations of several noninvasive diagnostic methods,“‘* invasive hemodynamic measurements still have to be performed in a significant number of patients. 13,14 Continuous-wave Dop- pler tracings of physiologic pulmonary regurgitation (PR) are highly promising tools because this flow is directly related to the pressure gradient between the pulmonary artery and the right ventricle by the Bernoulli equation. This physical relation led us to hypothesize that a modification of RV pressure could modify the regurgitant flow pattern. To test this hypothesis, the present study was designed to systematically search for the presence of a pulmonary regurgitant jet in patients with inferior wall acute myocardial infarction and to compare the modifications of the flow pattern with invasive hcmo- dynamic data.

:rom the Department cf Cardickx~y, Saint-Antoine Lnlverslty ks ta Scirt-Artaine Medkci Sciool. and the leoarimcr: oi Curd-o, P

i-

gy; Br~)ussais-HBtel-Dleu University Hcspital, Paris, F,ance. Manubpt received July 29, 1994; rewsec manuscript received and accepted November 3, 199d.

Address for reprints: Ariel Conen, MD, Deportment 01 Cardiob

YY, Saint-Ar:torne University Hospital, 184 Rue du FoucJsu:g Sa’r+ Antoine, 75571 Paris Ccdex 12. France.

METHODS Study group: From January 1990 to January 1992, all

patients admitted to the coronary care unit within 24 hours of the onset of an inferior wall acute myocardial infarction were included in the study. The inclusion criteria were: (1) prolonged chest pain (>30 minutes); (2) electrocardiographic evidence of 21 mm (0.1 mV) ST- segment elevation in 22 inferior leads (II, Ill, and aVF) with subsequent Q-wave formation; (3) more than a twofold increase in plasma creatine kinase; and (4) sinus rhythm at the time of hemodynamic and Doppler evalu- ation. The exclusion criteria were previous myocardial infarction, clinical evidence of obstructive pulmonary disease or severe PR, significant pulmonary hyperten- sion, severe supraventricular or ventricular arrhythmias, and atrioventricular block. Sixty-two consecutive patients were evaluated: 9 patients were excluded according to criteria mentioned, 2 patients died shortly after admission, 2 patients had atria1 fibrillation, 2 patients had second-degree atriovcntricular block, 3 patients had a concomitant anterior wall involvement or a history of previous myocardial infarction. Of the 53 remaining patients, a measurable PR was recorded in 48 (91%) (24 men and 5 women in group 1 and 18 men and 1 woman in group 2, mean ages 58 +I 12 and 56 f 11 years, respectively) who underwent further analysis: 29 patients in group 1 with hemodynamically proven RV involvement (RV+) and 19 in group 2 with inferior myocardial infarction but without RV involvement (RV-).

Doppler analysis: DATA ACQUISl'fIOh': Doppler echocardiography was performed within 24 hours of admis-

CCXIUAR” ARTiiZY DISEP.SC/DOPFLFR DtrTCTIOI\; Cl WI IT Vr,l\. IRlCtJlAR NTAXTIOI\; 425

sion, just before right-sided cardiac catheterization. Two- dimensional and Doppler echocardiograms were recorded using a commercially available imaging system, VingMed-Diasonics CFM 700 (Horten, Norway). The 2 MHz Pedoff probe was systematically placed in the left parastemal position to record pulmonary flow and detect physiologic pulmonary regurgitant flow by a careful step- by-step sweep of the RV outflow tract. PR had to be recorded throughout the entire diastole as a positive Row spectrum during normal respiration. Continuous-wave Doppler tracings and standard electrocardiographic lead 11 were simultaneously recorded at a speed of 100 mm/s. The entire Doppler cchocardiographic examination was recorded on VHS video tape with a Panasonic AG-6300 video cassette recorder for further off-line analysis.

R~OW PATTERNS: The normal pattern of physiologic regurgitant flow velocity is well characterized.is With regard to modifications in the compromised right ventricle, according to a pilot study we conducted in patients with constrictive pcricarditis, we anticipated the presence of an abrupt decrease of the jet velocity in early diastolc, reaching the zero line before the “a wave” or followed by a velocity increase after the a wave. The a wave was recorded as a posterior deflection in the regurgitant velocity profile, concomitant with a decreased jet velocity. The a wave occurred just after the P wave on the electrocardiogram.

MEASUKEMEKTS: The following parameters were determined: peak early diastolic velocity of PR (Vmax), minimal velocity of PR in mid-diastole before the a wave (Vmin), the Vmin/Vmax ratio, and pressure half-time of PR (PHT,,,). PHT,, represents the time required for the transpulmonary velocity to fall from its peak (Vmax) to Vmax/&. Echocardiograms were analyzed by experi- enccd echocardiographers who were unaware of the clec- trocardiographic and hemodynamic findings. All quantitative Doppler measurements and calculations were obtained olI-lint by 1 experienced observer (AC) who

was unaware of the clinical and hemodynamic findings. Three values for each parameter were averaged. In the presence of beat-to-beat marked variations, only the minimal values for Vmin/Vmax and PHT,, were considered.

Right-sided cardiac catheterization: After giving in- formed consent, all patients underwent right-sided cardiac catheterization within 24 hours of admission. Mean right atria1 pressure, RV early diastolic pressure, end- diastolic RV prcssurc, and systolic, diastolic, mean pulmonary artery, and pulmonary capillary wedge pressures were measured using a fluid-filled flotation cathe- ter (American Edwards, Irvine, California). Pressures were recorded simultaneously with the elearocardio- gram at paper speeds of 25, 50, and 100 mm/s. Then, cardiac output and index were determined. Three deter- minations for each parameter were made and the results averaged. Right atria1 pressure tracings were analyzed to determine the presence of a noncompliant pattern, according to the method of Lopez-Sendon et al.14 The presence of an RV diastolic dysfunction was indicated by the presence of an RV “dip-and-plateau” pattern, defined as a diastolic plateau grcatcr than one third of the systolic RV pressure. All pressure tracings were analyzed by 2 independent observers who were unaware of the patients’ clinical history. Because we intended to compare the invasive and Doppler pulmonary artery to the RV diastolic pressure gradient, we defined RV involvement as: (1) the presence of a right atrial noncompliant patterni or an RV dip-and-plateau pattem,7 and (2) a disproportionate elevation of right-sided filling prcssurc relative to left ventricular filling pressure (mean right atria1 prcssurc 210 mm Hg and RV end-diastolic to pulmonary capillary wedge pressure ratio 20.8.i3-i8 According to these hemodynamic criteria, the study pop- ulation was divided into 2 groups: group 1 (RV+) and group 2 (RV-).

Other parameters: CLINICAL. DATA: The presence of systemic hypotension (systolic arterial pressure 190 mm

Hg) and elevated jugular venous pressure suggesting RV involvement were systematically searched at admittance. ECG u ECG u

I I mmHg 0.4 s 0.4

mmHg ELEC171OCARDKXK4PHAPHlC DATA:@@

precordial leads (V,,, V,,, and V,,) were systematically recorded, and RV involvement was suspected when an ST-segment elevation 21 mm in V,, was prcsent.‘s~‘y*20

ECHOCARDIOGRAPHICDATA: RV dilatation was graded as absent or present when RV mid-diameter to left ventricular mid-diameter ratio was a.9 using apical or subcostal 4-chamber views. RV free wall motion abnormalities were defined as normal, hypokinetic, akinetic, or dyskinetic. The presence or absence of paradoxical systolic motion of the septum anteriorly toward the RV cavity was noted.

FIGURE 1. Hemodynomic tracings /upper pane/s) and Doppler pulmonary regurgi- totion tracings //ower pane/s] from o patient with /lefi panels) and in another patient without (right pane/s) right ventricular (Rv) involvement. ECG = electrocordi- ogrom; PA = pulmonoty artery.

LEl=T-SIDED IlEART CATHETERIZA- Tim: Two to 15 days after admission (mean 10 f 3) left ventricular angiography and coronary angiography were

426 IHt AMtKICAN JOUINA. OF CARDICIOCW VOL. 7.5 MARCI I 1, i99.5

method. RV involvement was suspected in the presence of right coronary artery occlusion or right coronary artery stenosis 270%, proximal to RV free wall branches.

Statistical analysis: All values are expressed as mean f SD. Qualitative variables (presence of clinical signs suggesting RV involvement, ST-segment clcvation in V,,, RV dilatation, RV wall motion abnormality, and PR) in patients with or without RV infarction were compared by chi-square analysis. For hcmody- namic and Doppler quantitative variables. the nonparametric Mann-Whitney test was performed. Univariate analysis and multiple logis-

Group 1 RVt

Parameters (n = 29)

Pressures [mm Hg) Mean right atrial 10.1 * 4.8 Systolic RV 25.0 * 6.0

5.8 * 4.1 RV early diastolic

RV end-diastolic 13.1 2 4.9

Systolic pulmonary artery 24.6 f 5.6 Diastolic pulmonary artery 12.8 e 4.3

18.0 + 4.5 Mean pulmonor artery Pulmonary cap11 ory wedge 7 13.5 t 4.2

Cardiac index (L/min/mg) 2.65 -t 1.20

Valuer ore expressed as mean + SD RV = right ventricular.

Group 2 RV-

(n = 19)

7.3 zt 2.7 27.0 zt 7.0

4.4 * 3.0

8.9 zt 3.1 27.6 TZ 7.2

12.6 * 4.5 18.6 e 5.0

14.2 c 5.0

2.50 5 0.56

p Value

<O.OOl NS

<O.OOl

<O.OOl NS

NS

E

NS

performed. Global left ventricular ejection fraction was calculated using the Dodge

TABLE I Hemodynamic Data in Patients With Inferior Wall Acute Myocardial

Infarction With (RV+) and Without (RV-) Right Ventricular Involvement

tic regression analysis were used to-deter&e whether clinical, electrocardiographic, hemodynamic, and Dop- pler echocardiographic findings were significantly associated with RV involvement. Statistical calculations were made by using SPSS software for Macintosh. Differ- ences were considered statistically significant at p ~0.05.

RESULTS There were no differences between the 2 groups with

regard to age, sex, thrombolysis (61% and 64%), delay of intervention (7 f 7 hours in the RV+ group and 4 f 4 hours in the RV- group), creatinc kinase peak (1,089 f 827 and 909 f 820), and left ventricular ejection fraction (53 f 11 and 51 f 11). Antianginal and antithrom- botic therapies were similar in both groups and were unchanged between Doppler echocardiographic and hemodynamic examinations.

Right-sided cardiac catheterization: By definition, right heart filling pressures were elevated in group I patients, whereas pulmonary pressures and cardiac index were not statistically different between the 2 groups (Table I). High-quality right atria1 pressure tracings were available in 43 patients (26 RV+ and 17 RV- patients). Twenty- five patients had a right atrial noncompliant pattern (all in group 1) and 18 had a normal right atrial pressure tracing. One patient with a normal right atria1 pressure tracing had an RV dip-and-plateau pattern and was included in group I. Among the 5 patients (3 in group 1 and 2 in group 2) with suboptimal right atrial pressure tracings, the 3 group 1 patients had RV dip-and-plateau and the 2 group 2 patients had normal RV pressures and morphol- ogy. In all, an RV dip-and-plateau pattern was present in 23 group 1 patients (79%) and in no group 2 patients.

Coronary angiograms: The coronary angiograms of the 29 group 1 patients demonstrated a signiEcant (270%) stenosis of Ihe right coronary artery in 20 patients and an occlusion in the remaining 9 without any collaterality from Ihe left coronary artery. Right coronary artery involvement was proximal to the Erst RV branch in 27 patients, whereas a thrombus was located just beneath the RV branch in 2, a Ending compatible with the migration of a proximal thrombus. Among 19 group 2 patients, 15 had a critical stenosis of the right coronary artery, 2 had a significant stenosis of the left circumflex artery, and 2 had normal coronary angiograms. Among the 15 group 2 patients with right coro-

nary artery involvement, only those having a significant stenosis proximal to the RV branch had collaterals from the left coronary artery.

Pulmonary regurgitation flow patterns: The pulmonary regurgitant flow v&city pattern differed greatly in patients with and without RV involvement (Figure 1, lower left panel). In patients with RV involvement, the pulmonary regurgitant flow pattern exhibited a rapid rise in flow velocity to a peak level, followed by an abrupt dcccleration in middiastole, and reaching the zero line before the a wave or followed by a velocity increase before the a wave. This pattern was observed mainly during inspiration in 18 group 1 patients (62%). In the 11 remaining group 1 patients, this characteristic pattern was present throughout Ihc entire respiratory cycle. In the absence of RV Involvement, the pattern of physiologic pulmonary regurgitant flow is characterized by a rapid increase in the llow velocity, followed by a gradual deceleration until the next pulmonary valve opening (Fig- ure 1, lower right panel). A clear velocity decrease in the regurgitant velocity pattern is usually recorded after atrial contraction.

There was no signiEcant difference between Vmax values in both groups: 1.35 f 0.26 m/s in group 1 and 1.45 f 0.37 m/s in group 2 (p = NS). Conversely. Vmin was significantly lower in group 1 patients (0.46 f 0.13 vs 0.86 f 0.34 m/s, respectively; p <O.OOl). Therefore, the Vmin/Vmax ratio was lower in group 1 (0.34 f 0.07 vs 0.59 + 0.13, respectively; p <O.OOl). The PHT,,, was significantly shorter in group 1 (91 i 31 vs 214 + 57 ms, respectively; p <O.OOl). In 4 group 1 patients, the PHT,, was ~60 ms and the pulmonary regurgitant velocity pattern was characterized by an interruption of the flow during the ventricular rapid filling wave in mid-diastolc (zero flow).

The diagnostic accuracy of various cutoff values for PHT,,, (<130 or 150 ms) and Vmin/Vmax (10.4 or 0.5) arc summarized in Table II. Figure 2 illustrates the clear distinction bctwecn patients with and without RV involvement when PHT,,, 1150 ms was used as the cutoff value. Figure 3 shows how accurately Vmin/Vmax 10.5 characterized the 2 groups. The best diagnostic yield was obtained when combining these 2 Doppler- derived indexes.

Other evidences of right ventricular involvement: CLIN- ICAL DATA: Thirteen group 1 patients (45%) had clinical

CCRONARY AR1 r KY I%-A:I-,‘I:C)+I I-? D”ECTI01 OF K <;I I : ‘/~NTRICJ!AR lt~rAt?C: I!ON 427

I TABLE II Diagnosis of Right Ventricular Involvement in 48 Patients With Acute Inferior Wall Myocardiol Infarction (according to hemodynomic classification]

Positive Negative Sensitivity Specificity Predictive Predictive Accuracy

VI (“V Value (“A) Value (%) VI

Electrocardiography ST-segment elevation 65 95 95 66 77 V,, >l mm

Echocardicgrophy RV dilatation 57 90 a9 58 70 RV wall motion 33 91 83 47 56

abnormalities Doppler

PHT, ~150 ms 100 84 91 100 94

Vmin/Vmox SO.5 100 63 81 100 PHT, ~150 ms and 100 89 94 100 ;z Vmin/Vmox CO.5

PHT,, < 130 ms 83 89 85 Vmin/Vmax 50.4 79 95 2 z 83 PHT,, ~130 ms and 66 100 100 66 79

Vmin/Vmox SO.4

PHT,, = pressure half-time of pulmonary regurgitation; RV - right ventricutor; Vmin/Vmox = lowest mid-diastolic to peak early diastolic velocity ratio

signs suggesting RV hemodynamic compromise, whereas no group 2 patient had such findings (p <O.OOl).

ELECTROCARDIOGRAPHIC RESULTS: Nineteen group 1 patients (66%) and 1 group 2 patient (5%) had 21 mm ST-segment elevation in lcad V,, (p <O.OOl). The diagnostic accuracy of electrocardiographic findings compared with hemodynamic criteria is indicated in Table Il.

ECHOCARDIOGRAPHIC FEATURES: Technically good echocardiograms were obtained in 46 of 48 patients (27 from group 1 and 19 from group 2). RV cavity was enlarged in 17 group 1 patients (59%) and in 2 group 2 patients (10.5%) (p ~0.01). The RV free wall was considered normal in 18, hypokinetic in 5, and akinetic in 6 group I patients. Paradoxical systolic septal motion was present in 3 group 1 patients. In group 2, only 2 patients had mild hypokinesia of the RV free wall (p ~0.01 vs group 1). The diagnostic value of RV dilatation and of the presence of RV wall motion abnormalities is shown in Table II.

Relation between Doppler parameters and noninvasive diagnostic tools for right ventricular invakment: When patients were classified as having RV involvement according to nonhcmodynamic diagnostic classifications (clinical, electrocardiographic, and echocardiographic), the diagnostic impact of PHT- PK 1150 ms and Vmin/Vmax SO.5 was still accurate (Table III). The results were similar when using only 1 criterion, such as PHT- t,a 5150 ms (data not shown).

Multiple logistk regression analysis: When clinical, electrocardiographic, and Doppler echocardiographic variables were analyzed using a step-by-step multiple logistic regression analysis, the strongest predictor of RV involvement was PHT,,,. PHT,,, could clas- sify RV involvement with a diagnostic accuracy of 94% (sensitivity 97% specificity 89%). An association with the Vmin/Vmax

ratio enhanced the diagnostic yield by increasing the specificity, with no significant change in sensitivity and diagnostic accuracy (95% 97%, and 96% respectively). None of the other variables that were significant predic- tors of RV involvement in the univariate analysis added any further predictive power above that contributed by PHT,,. Logistic regression analysis was also performed using the combination of the 2 cutoff values, PHT,,, 1150 ms and Vmin/Vmax 10.5. Again, specilicity (89%), sensitivity (MY%), and accuracy (96%) were high. Thus, in our study, the Doppler characteristics of PR were able to independently predict RV involvement, even when con- trolling for clinical and electrocardiographic variables.

p < 0.001 t t

. .

RV+ RV-

DISCUSSION The present study indicates that in a selected series

of patients with inferior wall acute myocardial infarction, pulmonary regurgitant flow tracings arc modified in the case of RV involvement and that these modifications could be used as a diagnostic tool: a hemodynami- tally proven RV involvement was constant when PHT,, was 1150 ms or Vmin/Vmax was 10.5. In addition, these

0.8 :

$ 0.6 ~ 0.5 - - -

+o 1 to. - - -

.5 0.4 D 2 0.2 a

0.0

RV+ RV-

FIGURE 2. The pressure halftime of pulmonary regurgitation (PHI ) in patients with (RV+) and without (RV-) right ventricu-

FIGURE 3. The lowest mid-diastolic to peok early diastolic

lar (I!+) . mvolvement. A cutoff point value for PHT vebcity ratio (Vmin/Vmox) in patients with (RV+) and without

~150 ms classifies potients with RV invdvement (sensitivity 7

(RV-) right ventricular (RV) invdvement. A cutoff point value 00%, speci-

ficity 84%). The vertica/ bon represent the SD and their centers for Vmin/Vmox <OS classifies patients with RV involvement

the meon. (sensitivity lOO%, specificity 63%). The vertical bars represent the SD and their centers the meon.

428 TI iC A,,“V\CRICAIU JOUKNAL OF CARDIOIOGY” Vol.. 75 ,&+ARCH , 1995

parameters were found to be better predic- tors of RV involvement than clinical, elec-

TABLE III Diagnostic Accuracy of Doppler-Derived Parameters of Pulmonary Regur- gitatlon in Patients Classified According to Clinical, Electrocardiographic, or

trocardiographic, or cchocardiographic find- Echocardiogrophic Signs Suggesting Right Ventricular Involvement

ings. PHT, <I 50 ms and Vmin/Vmax 50.5

Positive Negative Sensitivity Specificity Predictive Predictive Accuracy

1%) (%I Value (%) Value (“A) (%)

Hypotension or 84 57 68 76 71 elevated jugular venous pressure

ST-segment elevation 95 57 61 94 73 in VAR

RV dilatation 84 52 53 83 65

Abbrewotions 0s in Table II.

Hemodynamic features of right ventricular infarction: Among several hemodynamic parameters that have been evaluated in patients with RV infarction, the best diagnostic accuracy has been obtained with the combination of a disproportionate increase of right atrial’4*20*2’ or RV end-diastolic pressure ‘.‘3,‘8 relative to left ventricular cnd- dias;olic or pulmonary capillary wedge pressure, and the presence of a right atria1 pressure noncompliant pattern.14 The presence of a characteristic RV dip-and-plateau pattern has also been reported as an accurate, although not specific, criterion for RV i17farction.‘8,2’-‘4 The accuracy of the hemodynamic criteria used in the present study to diagnose RV involvement was confirmed by coronary angiographic data. All group 1 patients had significant stenosis or occlusion of the right coronary artery proximal to the first RV branch.

heart may unmask the characteristic Doppler pattern of RV dysfunction.

RV infarction is frequently associated with transient ST-segment elevation in right precordial leads.6~‘s~20 In our series. the presence of ST-segment elevation 21 mm in lead V4R had lower sensitivity (6.5%) and diagnostic accuracy (77%) but higher spec’ficity (95%) than those reported by others. 5~‘6 This discrepancy may be related to several factors. First, we had to exclude 9 patients from our initial group because of rhythm disturbances or early death. Second, our patients wcrc hospital&i soon after the onset of chest pain: 62% had thrombolyt- ic therapy and only one third of the group 1 patients had a right coronary alery occlusion at the time of coronary angiography. Third, the diagnostic accuracy of electrocardiographic Endings for RV infarction depends on the cutoff value used for ST-segment elevation in right precordial leads (0.5 or 1 mm). &I4 Finally, ST-segment elevation in V,, may be transient26 and is not specific for right coronary artery stenosis or occlusion.27

Hemodynamic determinants of pulmonary regurgitant jets: In diastole, minimal defects in the coaptation sur- faces of the pulmonary valve establish a communication between the pulmonary artcry and the right ventricle and, thus, create a pressure gradient. The global gradient is the difference hetwecn the passively decreasing diastolic pulmonary artery pressure and the increasing diastolic RV pressure. PRs are determined by local gradients through the Bernoulli equation.‘s Viscous energy loss- cs within the valves can usually bc neglected because the surface of coaptation has a small width. However, the pulmonary regurgitant velocit@ which are lower than expected (Figure 1) from the pulmonary artery-RV pressure difference could be a consequence of viscous pressure loss. The pressure recovery within the cavity, which is the difference between the local pressure inside the jet and the chamber pressure, can probably be neglected since it is significant only in the case of a non- turbulent jet or severe regurgitation. For these reasons, we have hypothesized that (1) the local gradient is almost equal to the global gradient, and (2) in patients with a normal pulmonary vascular bed, the pulmonary regurgitant jet is mainly dctcrmined by the RV diastolic pressure curve and could be used for determining modifications of the latter.

Diagnostic value of Doppler echocardiography and other noninvasive tools in detecting right ventricular involvement in patients with inferior wall myocardial infarction: Using nonimaging continuous-wave Doppler echocardiography, we were able to record PR in 91% of the patients, and PR was detected to the same extent in patients with or without RV involvement. A shortened PHT,, directly reflects the decreased pressure gradient between pulmonary artery and right ventricle in mid- diastole. The characteristic pattern of pulmonary recur- gitant flow was observed predominantly during insp’ra- tion in 61% of patients. This suggests that in mild RV dysfunction, the inspiratory increase in right heart diastolic filling pressure with increased flow into the right

In our study, RV cavity enlargement occurred significantly more often in patients with RV infarction, but >40% of patients with hemodynamically proven RV involvement did not have any significant echocardiographic abnormality. Dell’Italia et al” reported simila’ results in a series of 14 patients with and 39 without hemodynamically proven RV infarction. The use of RV wall motion abnonnalities in detecting RV involvement had a sensitivity of 82% but a specilicity of 62%; the positive predictive value was 41%.” Thus, the higher sensitivity than that reported in our series was balanced by a lower specilicity. Echocardiography has low sensitivity and specificity in detecting small RV involvement.28 Furthermore, as reported recently by Laster et a12’ in an experimental study, early rcpcrfusion after l- and 4-hour right coronary occlusion may result in prompt recovery of regional and global RV function, whereas RV end-diastolic pressure is still elevated.

Finally, one has to be cautious when comparing the diagnostic yield of these different diagnostic tools; iso- topes evaluate RV perfusion (technetium-99m) or RV systolic function (radionuclide angiography) when invasive or noninvasive hemodynamics detect RV diastolic dysfunction. In fact, the term RV infarction rcprcscnts a spectrum of diseases and includes transient ischcmic myocardial dysfunction, “stunning,” and localized myocardial cell necrosis (the latter determined only by autopsy).‘-3J3

(;OKONARY ARltKY DISEASF/I~OPPLER DETFClION 0 KIGHT VENTRICUIAK INtAKC IION 429

Differential diagnosis of Doppler findings: The equal- ization of diastolic pressure and an RV dip-and-plateau configuration may be observed in different clinical con- ditions, such as restrictive cardiomyopathy and pericar- dial constriction. We previously investigated the diagnostic yield of pulmonary regurgitant tracing analysis in patients with constrictive pcricarditis. In a series of 13 patients compared with 45 normal or unaffected controls, we found that PHT,,, and the ratio of the lowest mid- diastolic to peak early diastolic pressure decrease were significantly lower in patients with restrictive ventricular pathology (unpublished data). In our series, no patient had severe PR that could increase the rapid tilling wave and simulate RV dysfunction. In such patients, a continuous decrease in the velocity of regurgitation is usually observed and the deceleration is maximal at end- diastole.

Study limitations: One limitation of our study is related to the definition of the group. We studied a selected series of patients with RV myocardial infarction because we could only include patients in sinus rhythm with Doppler-detectable PK. Only 9% of our patients had no detectable PR, whereas Masuyama et al”” reported that 46% of their patients had undetectable PR. The high rate of pulmonary regurgitant flow recorded may be attrib- utable to the use of a nonimaging Pedotf 2 MHz probe and the improvement in technology of more recent echo machines (which can detect pulmonary regurgitant flow with greater sensitivity than color-guided probes). A limitation of our study is that right-sided cardiac catheterization and Doppler echocardiographic studies were not performed simultaneously. However, patients underwent cardiac catheterization within a few hours of the Doppler echocardiographic examination. Finally, we did not study RV inflow velocities in order to better characterize RV filling abnormalities in the acute phase of RV infarction.

Clinical implications: In this series of patients with inferior wall acute myocardial infarction, a qualitative and quantitative analysis of pulmonary regurgitant tracings allowed the diagnosis of hemodynamically proven RV involvcmcnt. Our results suggest that a complete Doppler echocardiographic examination should include pulmonary regurgitant detection. Furthermore, indica- tions for emergency echocardiograms in patients with acute myocardial infarction could be expanded. This approach is less aggressive than right-sided cardiac catheterization and more available than nuclear imaging at the bedside in coronary care units.

1. lsner JM, Kobcrts WC. Kight ventricular infarction complicating lcli vcnlricu- lar infarction secondary to coronary heart disease. Frequency. Iocatmn, associated findings and rigmlicance from analysis of 236 necropsy patients with acute: or healed myocardial infarction. Am J Curdiol 197&42:8X.5-X94. 2 Radiff ND, Hackel RB. Combined right and left ventricular infarction: patho- genesis and clinicopathologic correlations. Am J Cardiol 19X%45:217-22 I. 3. Andenen I IR. Frdk E, Nielsen D. Right ventricular infarction: frequency, si7e and topography in coronary anery disease: a prospective study comprising I07 consecutive autopsies from a coronary cart unit. J Am CON Curdiol 1987; IO: 1223-1232. 4. Cabin HS, Cluhh KS. Wackers FJT, tit BL. Kight ventricular myocardial infarction with anterior wall left ventricular infarction: an autopsy study. Anr Heart J 1987;113:16-23.

5. lsner JM. Right ventricular myocardial infarction. In: Konstam M.4, Isner J!vl, edb. The Right Ventricle. Boston: Kluwcr Academic, 1988:87-129. 6. Zehendcr M, Kasper W. Kaudcr E, Schiinthaler M. Geibcl A, Olcchcwtki .M, Just H. Right ventricular infarction as an independent predictor of prognosis after XUIC inferior myocardial infarction. N Eng/ J Med lYY3:328:981-988. 7. Ehrardt I.R. Sjogren A, Wahlbcrg 1. Single right-sided prccordial lead in the diagnosis of right ventricular involvement in inlixior myocardial infarction. /\nr Ilearr J lY76:Yl:S71-Sib. 8. Rigo I’, .Murray M, ‘Taylor DK. Weisfeldt M. Kelly DT. Strauss HW. Pitt B. Kight ventricular dysfunction detected by gated scinuphotography in patients with acute mierior myrrardial infarction. Cin ulation 1975:52:268 274. 9. Tohinick E, Schelbert HR. Henning H. LeWintcr M, Taylor A, Ashbum WI., Karliner JS. Right venrricular ejection fraction in padems wth acute anterior and inferior tnywardial infation aswssed by radionuclide angiography. Cirmhrion 1978;57: 1078 - 10x4. 10. D’Arcy B, Nanda NC. Two-dimensional echwardiogmphic icarures of right ventricular infarction. Cbrufarinn lY82:65: 167-173. 11. Antunes ML, Johnson LL. Seldin DW, Bhatia K, Tresgallo ME, Grecr~apan RL, Vaccarino RA. Rodney RA. Diagnosis ol right ventricular acute myocardial infaction by dual isotope thallium-201 and indiun- I 11 amimyosm SPECT imaging. Am J Cordial lY92;70:42&43 I. 12. Asaw H, Sane ‘I‘. ‘Tsuboi H, Sass H. ‘l‘akwhima K, Miyataki Y. Okumura K. Hashimoto H, Ito T. Diagnosis of nghr ventricular iniarctmn by overlap images of simultaneous dual emission computed tomography using technetium-YYm pyrophoaphate and thallium 201. Am J Curdml 1993:71:%x)2-x)8. 13. Cohn J.U, Guiha Nil, BrcxJer Ml. Lima, CJ. Right ventricular infarction. Clint- ical and hemwlynamic fcaturw. Am J Cardrol 1974;33:209-214. 14. Loper-Sendofi J, Coma-Can& I, Gamallo C. Sensitivity and bpcciticity of henmdynamic criteria in the diagnosis of acute right ventricular infarction. Crrw- /ur,on 3981;64:515-525. 15. Candell-Riera J, Figueras J, Vale V. Alvarez A, Gutuxel L. Conadellas I, Cin- ca J. S&s A, Rius 1. Right ventricular mfarction: relationships between ST-seg- mcm clcvation in V,,< and hemodynamic, acintlgrapblc and cchocardiographir tind- ings in patients with acute infenor myocaxhal illfarcrion. Anr llerrrr .I lY8l; 101: 281-287. 16. Baigrie RS. Hay A, Morgan CD, Rakowrki H, Drohac M. !vlclaughtm P. ‘lhe spt~rum oi right v~~tncular involvcmem in inierior wall mywardial infarction: a clinical. hemodynamic and nolimvasive study. J Am Co// Curdio/ 1983; I : 1396 1404. 17. Dell’lratia LJ, Starling .MR, Crawford M, Bores BL, Cbaudhwi TK, O’Rourke RA, Hey1 B, Amon KW. Right ventricular iniarction: identilication by hcmody- namic me~wremettts before and after volume loading and corrrlation with nomn- u&e techniques. J Am Coil Cardiol 1984:4:93 t-939. 18. Lloyd EA. Gersh BJ, Kennelly BM. Hemodynamic spwxrum of “dominant” right ventricular infarction in I9 patients. Am J Cardiol lY81:48: 10161022. 19. Klan 110, ‘l’ordjnla~l T. Ninio K, Sareli I’. Oren V. Lang R, Gefen J, Pawner C, di Segni E. David D, Kaplimky E. 1110 early recognition uf right vcnuicular infarctiox diagnortic accuracy of the electrocardiogrephic V,, lead. Ctrcu/u/ioo 1983;67:558 565. 20. LopwScndon 1, Coma-Canelld I. Ascascna S, Seoane J. Gamallo C. Elecrro- cardiogmphic findings in acute right ventricular iniarction: scnsitiwty and apeci- licity of clecuwardiographic alterations in right precordial leads V,,, V,,, VI, V2 and V3. J Am Co/l Cord& lY85;6:1273- 1278. 21. Daubert JC, Deplace C. Bourdomw C. Pony JC, Gouffautr J. I.‘infarctub du ventricule droit: diagnostic htmodynamique. Corr&tions anatomiques. Arch Mu/ Coeur lY77:70:243-255. 22. Coma-Can& I, Lopu-Sendon J. Ventricular compliance in ixhemic right ventricular dysfuncuon. Am J CordioL 1980:45:555 561. 23. Jensen DP, Gmlshy JP. Oliva PB. Hemodynamic pattern rcacmbling p&cardial constriction after acute inferior myocardial infarction with right ventricular infarction. Am J Cardiol 1978:42:858-X61. 24. Gold&n JA, Bar&i 8, Roaamong TL, Eisenberg PR, Jaffe AS. Determinants of hemndynamic comprormse with severe right ventricular infarction. Cirwlatron 1990;82:3SY-36X. 25. Weyman AE. Principlcb and Practice of Echocardiography. 2nd ed. Phdadel- phia: Lea & Febiger, 1994: l&%200. 26. Braat SH, Brugada I’, deZuwm C, Cwnegracht J&I, Weltens HJJ. Vatuc ol electrcardiogram in diagnosing right ventricular involvement in patients with an acute inferior wall myocardial infarction. Br //eat-f J lYX3;4Y:368-372. 27. Krueger DW, Morrison DA, Buckner K. K&y K. Iindcnietd Jn. IS ST elevation the only electrcardiognphic response of the ischernic right vemriclc? Am J Cardiol 1992;67:643645. 28. LopzSendon J. Garcia-Femandez .X4/\, Coma-Canella 1. Yanguela MM, Banw lo\ F. Segmental right ventricular function aher acute mywardial infarction: two- dimensional echocardiographic study m 63 patients. Am J Cordial 1983;5 1:39%396. 29.li~wr SB. Ohnishi Y. Saflitz JE, Goldstein JA. Effects of reperiusion on iwhc- mic right ventricular dysfunction: disparate mechanisms 01 beneli r&led to dura- tion oi i.schcmia. Cirfxlatron 1994;90:1398 1409. 30. Masuyama T, K&ma K, Kitabatake A. Sam H, Nanto S. lnouc 41. Continu- ous-wave Doppler echocardiographic detection oi pulmonary regurgitation and its application to rmnmvasive eslimation of pulmonary artery pressure. Cwculuru~,~ 1986;74:4X4-+‘)2.

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relations between doppler tracings of pulmonary regurgitation and invasive hemodynamics in acute...

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