Phasic coronary artery flow velocity determined by Doppler flowmeter catheter in aortic stenosis and aortic regurgitation

VALVULAR HEART DISEASE

Phasic Coronary Artery Flow Velocity Determined by Doppler Flowmeter Catheter in Aortic Stenosis and Aortic Regurgitation Shuzo Matsuo, MD, Mitsuhiro Tsuruta, MD, Motonobu Hayano, MD, Youichi Imamura, MD, Yoshiki Eguchi, MD, Takashi Tokushima, MD, and Shinsuke Tsuji, MD

Phasic coronary artery flow velocity was recorded in 14 patients with aortic regurgitation (AR), 4 with aortic stenosis, 61 with other heart diseases and in 2 normal subjects by means of a bidireetionai Doppler flowmeter catheter. The normal pattern of the phasic coronary artery flow velocity was characterized by a small forward flow during systole (S wave) and a large forward flow during diastole (D wave). The phasic coronary artery flow velocity in patients with AR showed increased S wave and decreased D wave. The area under the S-wave curve divided by the area under the D-wave curve (S/D ratio) in patients with AR increased (left coronary artery flow velocity 0.66 f 0.39, p <0.05; right coronary flow velocity 0.79 f 0.36, p
From the Department of Internal Medicine, Saga Medical School, Nabeshima, Saga, Japan. Manuscript received January 5,1988; revised manuscript received and accepted June 27, 1988. Address for reprints: Shuzo Matsuo, MD, Department of Internal Medicine, Saga Medical School, Nabeshima, Saga, 840-01, Japan.

linically, some patients with aortic valve disease have angina1pain in the presenceof normal coronary arteries.‘e4Such pain may be due to inadequate coronary flow caused by the hemodynamic changesthat characterize this disease,especially at the coronary orifice. A decreaseddiastolic coronary flow pattern has been reported in experimental studies of acute aortic regurgitation in dogs.5-8In human studies, electromagneticflowmeter measurementsof phasic coronary flow during open-heart surgery have shown results similar to those obtained in animal experiments.9 There are no reports on coronary flow patterns in consciousman with aortic valve diseasebecauseof the difficulty of measuring phasic coronary flow in the consciousstate. We have been studying flow velocity in the cardiac chamber and in various vesselswith a bidirectional Doppler flowmeter catheter and have found this approach to provide valuable hemodynamic information.10-‘6 In the present study we used a bidirectional Doppler flowmeter catheter to examine coronary flow velocity in consciouspatients who had aortic valve disease.

C

METHODS

Eighty-one patients ages20 to 69 years (48 men and 33 women) were studied. The patients were divided into 3 groups (Table I). Group I consisted of 14 patients with aortic regurgitation (AR) (6 men and 8 women). Group II consisted of 4 patients with aortic stenosis (AS) (2 men and 2 women). Two of these 4 patients had predominant AS combined with mild AR. Nonaortic valvular diseasecharacterized group III, which consisted of patients with coronary artery disease(31), mitral valvular disease(9), cardiomyopathy (7), congenital heart disease(7), other miscellaneousheart diseases (7) and 2 normal subjects (40 men and 23 women). Their age ranged between20 and 67 years with a mean of 50 f 10. All diagnoseswere establishedby meansof complete left- and right-sided cardiac catheterization and selective cineangiography. Coronary cineangiography failed to reveal significant stenosisof the coronary artery in patients with aortic regurgitation and in patients with aortic stenosis. Instantaneous phasic coronary artery flow velocity was measuredwith the bidirectional Doppler flowmeter catheter (Southwest Research Institute).17J8After the routine cardiac catheterization

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FLOW IN AORTlC

VALVULAR

D&EASE

TABLE I Coronary Artery Flow Velocity Recordings No. Group

Diagnosis

PtS

I II III Total

AR AS Normal AV

14 4 63

ai

Age Ws)

(“n”= 107) LMCA RCA

48f9 57fll 5ofll 50flO

4 41 53

a

10 1 43 54

AR = antic regurgitation; AS = aortic stenosis; AV = aortc valve; CFV = coronary flow velocity; LMCA = left main coronary artery; RCA = raght coronary artery.

study, the Doppler flowmeter catheter was inserted into the femoral artery. The catheter was advanced under fluoroscopic control to the ascending aorta and its tip was positioned at the ostium of the right or left coronary artery, or both, where measurementswere made. The technique used to position the catheter at the ostiurn of the coronary arteries was essentially the sameas that used for selectivecoronary arteriograms. The tip of the catheter was placed near the ostium of the coronary artery and not in its lumen. On many occasions,it was necessaryto reposition the catheter tip to avoid reflected signals due to aortic wall motion. The audio frequency signal was continuously monitored by meansof a loudspeaker. The flowmeter catheter was connected to a dual-frequency directional Doppler flowmeter (Parks Electronics Laboratory Model 909) and the output sig nals were recorded on a Mingograph unit at a paper speedof 5 or 10 cm/s. Phasic coronary artery flow velocity, lead II of the electrocardiogram and phonocardiogram at the third left sternal border were recorded simultaneously. Zero flow velocity was obtained by briefly disconnecting the input signal to the frequency meter, as zero frequency shift correspondsto zero velocity. Becauseit was difficult to place the tip of the cathe ter at the coronary ostium in some patients, both left and right recordings of coronary artery flow velocity could not be obtained in all of them. A total of 53 recordings of left coronary artery flow velocity and 54 of right coronary artery flow velocity were obtained (Table 1). RESULTS Normal pattern

FIGURE 1. Data from a 56.year-old man with mild hypertem SiOll.A,iWflIIOfthO ektrocardiogram, phanacardiiam at eorOnaryart~flOWVObCltY. thothirdstamalhordsrandloft B, ioad II ol the ekbocadogram, phonocardiiam at the thirdleftstemalbderandrtghtcoranaryarterytbwvebcity inthcrame~tient.LCA=kftcwonaryartery;RCA=right CoroMlyartwy.

of the phasic coronary

flow veki-

ty: Such a pattern was characterized by a small forward flow during systole (S wave) and a large forward flow during diastole (D wave). The peak of the S wave was small, approximately one fourth to one half of the peak of the D wave (Figure 1). Although the S wave of the right coronary artery flow velocity tended to be slightly larger than that of the left coronary artery flow velocity, essentially there was no difference between the right and left waveforms of coronary flow velocity. Coronary regurgitation

artery flow velocity in patients with aartii (group I): Markedly increased systolic

FlGURE 2. Coronvy arteq Gow vobcityina60-yoar-oldwoman withaartkregurgitation(souers IV). n, lead II of the e4eeocardiawanb ph?mowd~~ at thotldrdldlstomalborderand rlsM-~wveloeity.~, ~WhYfranthe=-P, .

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RGURE 3. A, lead II of the electrocarbogram, phonowdiogramatthethirdleftsternal bderand WarteryfiW velocity in a nomml SG-year-old woman. 6, Sl-year-old woman wlthawticregwgRation(seilers It). C, 99.year-old woman with aortlc mgwghth (sellers Ill).

D, 60.year-old woman with aortic regurgihtkn (sellers IV). R.C~.Art.FlowVeloc. = &ht coronarYartery~Wwlocity; I.cor.Art.Flowvebc. = left coronary artery flow velocRy.

CORONARY ARTERY FLOW VELOCITY IN

JA

I

FlGURE4. A,leadIIoftheelect==mF=bphonocanli~gramatthethirdleftstemal borderand coroMlr=tWfiW velocity in a normai S-year-old waman. B, 3G-year-old-man with aortlc stenods. c, s9-yearoldwomanwithaorticstenods. Abbrevlatbns as in Figure 3.

PATIENTS

WITH AORTIC STENOSIS

, B,

I

,

,

3LSB

3LSB

5. M. 56F

,c-

normal ANI

132/65mmHg K .M. 56M.

M.H.

59F

I

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CORONARY FLOW IN AORTIC VALVULAR MSEASE

flow (S wave) and decreaseddiastolic flow (D wave) were seen in this group, with a backward flow during mid-diastole observedin patients with severeAR (Figure 2). The peak S wave was larger than the peak D wave. Thesepatterns of coronary flow velocity were not seen in normal subjects. Compared with normal sub jects, increased S waves and decreasedD waves were seenon the recordings of patients with AR. As Figure 3 shows, these flow velocity patterns becomevery dominant in severeAR. Coronary

artery flow velocity in patients

pure AS. Figure 6 showsthe relation betweenS/D ratio and cineangiographicgrade of AR. There was a tendency toward increasedS/D ratio with increasedseverity of AR.

with aortic

stenosis (group II): Figure 4 shows the recordings of coronary artery flow velocity in a normal subject and 2 0 patients with AS who had 40- and 114~mmHg pressure 0 gradients between aorta and left ventricle, respectively. DecreasedS wave and increased D wave were seen in 0 patients with AS as compared with a normal subject. t.0 0 S/D ratio in patients with aortic valve disease: The 0 area under the S-wave curve divided by the area under 0 the D wave (S/D ratio) was calculated from the record0 0 0 ings of coronary artery flow velocity by using the model 0 Z-5 picture analyzer (Medical System Research). The 0.5 0 0 recording of left coronary artery flow velocity showeda 8 0 significantly increased S/D ratio in patients with AR 8 (0.66 f 0.39, p
1/

A

I. Cor Art Flow Veloc. , P
B

r. Cot-.Art. Fbv Woe , P(O.01 (

l

36: ratio FIGURE 5. A, S/D retio et the

inpetiembwithnomorbc law diseese (group Ill), peknts wRhaor6crogu+Wn(gmup I)andp&Mtswitheerticstemesls(gmupII).B,SIDretioefthe 0Asr

"9 aT I

li#lteorOnaryartaryllOWVObC-

ity ill group I, II end Ill. Vertkel l

bHSreprerantthOlllOallVdwi

standddovla6mASr=aor6c saomslsdmildcombir#dro-.

ok3

AS

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DISCUSSION

Angina pectoris is frequently seen in patients with severe aortic valve disease.im4 The incidence of angina pectoris in patients with significant aortic valve disease has been reported to be between 40 to 80% for predominant ASi,2J9 and 3 to 62% for predominant AR.‘,* Graboys et all reported the frequency of angina pectoris in 66 patients with predominant aortic valve disease. After dividing their patients into 3 groups, angina pectoris was found in 63% of 19 patients with predominant AS (group I), 62% of 29 patients with AR (group II) and 67% of 18 patients with combined AS and AR (group III). Associated coronary artery disease (275% luminal stenosis) averaged 20% for the entire group of 66 patients. This indicates that, in most cases, angina is not due to associated coronary artery disease. The mechanism of angina pectoris in AR has been explained by a decreased myocardial oxygen supply caused by lower coronary perfusion pressure during diastole and increased myocardial oxygen demand due to elevated end-diastolic volume,l whereas the mechanism of angina pectoris in AS has been explained by a decreased myocardial oxygen supply due to reduced coronary perfusion through a fixed stenotic valve orifice and prolonged left ventricular ejection time with corresponding clearance in diastolic filling period, and by increased myocardial oxygen demand due to increased wall tension.2,20 In animal experiments of AR, a pattern of increased systolic and decreased diastolic coronary flow has been reported5-7 The few methods that exist for measuring coronary flow in conscious man include the radionuclide method,*’ coronary sinus thermodilution method,22T23 gas clearance method24 and Doppler method.18,25,26Although most of these methods provide information only on mean flow, the Doppler method can measure instantaneous phasic coronary flow velocity. Folts et al9 made direct measurements of phasic coronary blood flow with an electromagnetic flowmeter during surgery in 8 patients with severe AR before and after replacement of the aortic valve. In their study, increased systolic flow and decreased diastolic flow were observed on the recordings of phasic coronary flow before surgery. The coronary flow pattern returned to normal after surgery. However, coronary flow was measured under open chest and anesthetized state conditions. To our knowledge, there has been no report on phasic coronary artery flow patterns in conscious patients with aortic valve disease. In the present study, a pattern of decreased diastolic and increased systolic flow was observed on the recording of coronary artery flow velocity in conscious AR patients that was similar to the findings seen in experimental AR and in patients with AR during surgery. The S/D ratio of the coronary artery flow velocity was much higher in patients with AR as compared with patients with nonaortic valvular disease. These changes in phasic coronary artery flow velocity could be explained by the following mechanism: in patients with dominant AR, the low-diastolic perfusion pressure leaves the epicardial vessels partially col-

lapsed. Thus, with the large increase in pulse pressure during systole, the epicardial vessels can accommodate more blood before the effects of mural and extramural pressure become restrictive.5 In our study, a tendency toward increased S/D ratio was also observed with the increase of severity of AR. These results are compatible with the explanation of the aforementioned mechanism in patients with AR. In cases with AS, we recorded the coronary flow velocity in only 4 patients. Because cases with AS are few, we could not state the exact characteristics of the phasic coronary artery flow pattern in such patients. However, the coronary artery flow velocities of 2 patients with pure AS showed decreased S wave, increased D wave and decreased S/D ratio when compared with a normal subject. In patients with AS, rapid jet stream through the stenotic valve in the aortic orifice could be the mechanism of reduced systolic flow and compensatory increase of diastolic flow. The Doppler flowmeter catheter used in our study measures phasic systolic and diastolic coronary flow velocity at the coronary orifice, but does not measure intracoronary flow. The availability of a small intracoronary probe (the microtip Doppler transducer DC 101 from Millers) enabled us to measure some phasic coronary flow velocities and to compare the results with those obtained with our methods. Although the absolute value of the flow velocity was slightly different between these 2 methods, the essential pattern of the flow velocity was almost identical. REFERENCES 1. Graboys TB, Gohn PF. The prevalence of angina pectoris and abnormal coronary arteriograms in severe aortic valvular disease. Am Heart J 1977,93:683686. 2. Basta LL, Raines D. Najjar S, Kioschos M. Clinical, haemcdynamic and coronary angiographic correlates of angina pectoris in patients with severe aortic valve disease. Br Heart J 197537:150-157. 3. Segal J, Harvey P, Hufnagel C. A clinical study of one hundred cases of severe aortic insufficiency. Am J Med 1956;21:200-210. 4. Bland EF, Wheeler EO. Severe aortic regurgitation in young people, a longterm perspective with reference to prognosis and prosthesis. N Eng/ J Med 1957;256:667-672. 5. Felts JD, Rowe GG. Coronary and hemodynamic effects of temporary acute aortic insufficiency in intact anesthetized dogs. Circ Res 1974;35:238-246. 6. Karp RB, Roe BB. Effect of aortic insufficiency on phasic flow patterns in the coronary artery. Ann Surg 1966;164:959-966. 7. Mizutani T. A study of coronary circulation in experimental aortic insufficiency with special reference to phasic coronary flow pattern. Jpn Circ J 1973;37;123133. 8. Feldman RL, Nichols WW, Pepine CJ, Conti CR. Influence of aortic insufficiency on the hemodynamic significance of a coronary artery narrowing. Circulotion 1979,60:259-268. 9. Felts JD, Rowe GG, Kahn DR. Young WP. Phasic changes in human right coronary blood flow before and after repair of aortic insufficiency. Am Hearf J 1979,97:21 l-215. 10. Benchimol A, Matsuo S. Continuous measurements of phasic aortic and coronary flow velocity during atria1 fibrillation in man. Am J Med 1971;51:466-

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