Normal coronary flow reserve in patients with mitral valve prolapse, a positive exercise test and normal coronary arteries

We studied 12 patients (eight females and four males), ages30–46 years, with echocardiographically documented mitralvalve prolapse and clinical suspicion of coronary artery disease,based on a history of chest pain (five patients), angina-likepain (three patients), a positive exercise stress electrocardiogram(12 patients) and a focally positive thallium-201 stress perfusionscan (three patients), who were referred for cardiac catheterizationand found to have normal coronary arteries. Ten patients withoutevidence of heart disease served as controls. In all mitralvalve prolapse patients, coronary flow velocity reserve wasdetermined successively in the left anterior descending, leftcircumflex and right coronary arteries as the ratio of the maximun(after intracoronary papaverine) to the resting mean coronaryflow velocity. Coronary flow reserve values were fairly similarin the mitral valve prolapse and control patients; all 12 mitralvalve prolapse patients had normal coronary flow reserve (3·5)in all three coronary arteries with no significant differencesamong the arteries tested Mean values ± 1 standard deviationof the coronary flow reserve (mitral valve prolapse vs controlpatients) were 4·7 ± 0·5 vs 4·6± 0·6 for the left anterior descending, 4·6± 0·4 vs 4·6 ± 0·3 for theleft circumflex and 4· ± 0·4 vs 4·4± 0·5 for the right coronary artery (all P=non-significant).The subsets of mitral valve prolapse patients with differentclinical ‘ischaemic’ manifestations were similarin terms of the calculated coronary flow reserve in all threemajor epicardial coronary arteries. In conclusion, this study demonstrated that an inadequate regionalcoronary flow reserve does not account for the clinical manifestationsof myocardial ischaemia and positive exercise tests in patientswith mitral valve prolapse and normal coronary arteries.     

Early results after mitral valvuloplasty for pure mitral regurgitation

In this study we present the results of 105 consecutive patientswith pure mitral regurgitation who underwent surgical treatment.In all patients mitral regurgitation was associated with mitralvalve prolapse: 54 patients underwent mitral valvuloplasty and51 patients mitral valve replacement. Clinical assessment and echocardiography were used as follow-upcriteria at one year after surgery. After mitral valvuloplasty,NYH A decreased from 2.7±0.8 to 1.1±0.7 (P<0.01)and workload capacity increased from 65±28% to 96±25%(P<0.001); left endsystolic atrial dimension and enddiastolicdimension decreased from 6.2±0.8 to 4.8±1.2 cm(P<0.001) and from 7.2±1.3 to 5.9±0.8 cm (P<0.01);ventricular contraction fraction did not change significantly. After mitral valve replacement, clinical and echocardiographicimprovement was significant but less remarkable than after valvuloplasty;ventricular contraction fraction fell from 39±7% to 29±8%in contrast to patients undergoing mitral valvuloplasty in whomno significant change occurred. Complications were rare in both groups though only a minorityof patients undergoing mitral valvuloplasty received anticoagulants.We conclude that mitral valvuloplasty in patients with puremitral regurgitation associated with mitral valve prolapse givesexcellent results, particularly regarding left ventricular functionwhen compared with the patients after mitral valve replacement.     

Early results after mitral valvuloplasty for pure mitral regurgitation

In this study we present the results of 105 consecutive patientswith pure mitral regurgitation who underwent surgical treatment.In all patients mitral regurgitation was associated with mitralvalve prolapse: 54 patients underwent mitral valvuloplasty and51 patients mitral valve replacement. Clinical assessment and echocardiography were used as follow-upcriteria at one year after surgery. After mitral valvuloplasty,NYH A decreased from 2.7±0.8 to 1.1±0.7 (P<0.01)and workload capacity increased from 65±28% to 96±25%(P<0.001); left endsystolic atrial dimension and enddiastolicdimension decreased from 6.2±0.8 to 4.8±1.2 cm(P<0.001) and from 7.2±1.3 to 5.9±0.8 cm (P<0.01);ventricular contraction fraction did not change significantly. After mitral valve replacement, clinical and echocardiographicimprovement was significant but less remarkable than after valvuloplasty;ventricular contraction fraction fell from 39±7% to 29±8%in contrast to patients undergoing mitral valvuloplasty in whomno significant change occurred. Complications were rare in both groups though only a minorityof patients undergoing mitral valvuloplasty received anticoagulants.We conclude that mitral valvuloplasty in patients with puremitral regurgitation associated with mitral valve prolapse givesexcellent results, particularly regarding left ventricular functionwhen compared with the patients after mitral valve replacement.     

Different mechanisms of mitral regurgitation in acute and chronic forms of coronary heart disease

Contradictory two-dimensional echocardiographic findings havebeen reported in relation to the role of prolapse of the mitralvalve and lack of systolic leaflet coaptation in mitral regurgitationsecondary to coronary heart disease. A prospective study of22 patients with chronic coronary heart disease and mitral regurgitationshowed the following: Inferior akinesia was detected in 14 (64%),fibrosis of the posteromedial papillary muscle in 10 (45%),and prolapse of the mitral valve in nine (41%). A combinationof the three signs was seen in six patients (27%). Lack of systolicleaflet coaptation was seen in only two patients, both withanterior myocardial infarction. When these results are comparedwith those reported in the literature, it is apparent that inacute coronary heart disease, lack of leaflet coaptation isfrequently visualized (P <0.0l) and fibrosis of the postero-medialpapillary muscle and prolapse of the mitral valve are lacking(P<0.01). A unitary explanation of all forms of mitral regurgitation incoronary heart disease is misleading; mechanisms of mitral regurgitationin coronary heart disease depend on the clinical presentation-acuteor chronic, the site of infarction, and the presence of cardiacdilatation.     

Comparison between regional myocardial perfusion reserve and coronary flow reserve in the canine heart

Diameter stenosis and flow reserve are indices of morphologicaland functional severity of coronary artery stenosis. Flow reservecan be determined at coronary arterial or at myocardial level.In the presence of functional collateral circulation, coronaryflow reserve and myocardial perfusion reserve may differ. We studied coronary flow, coronary flow reserve and myocardialperfusion reserve in an open chest dog model with intact collateralcirculation, before and after induction of coronary artery stenosis.Coronary flow was determined with perivascular ultrasonic flowprobes and myocardial perfusion reserve from digital angiographicimages, in the stenotic as well as the adjacent non-stenoticcoronary arteries. Before induction of a stenosis, a significant correlation existedbetween coronary flow reserve and myocardial perfusion reserveof the left anterior descending (r=0·59; P<0·005)and the left circumflex arteries (r=0·84, P<0·005).In stenotic arteries, coronary flow reserve and myocardial perfusionreserve decreased significantly (P<0·005), but inthe adjacent non-stenotic arteries coronary flow reserve wasnot affected Myocardial perfusion reserve in the non-stenoticadjacent left anterior descending artery decreased significantly(P<0·05) and no correlation was found between coronaryflow reserve and myocardial perfusion reserve, whereas in theadjacent non-stenotic left circumflex artery there was no statisticallysignificant decrease (4·1 ± 1·6 3·5± 1·4) but there was a good correlation betweencoronary flow reserve and myocardial perfusion reserve (r=0·85;P<0·005). This study demonstrates that, in the presence of a stenosisand functioning collateral circulation, coronary flow reserveis not a reliable predictor of myocardial perfusion reserve;both parameters provide mutually complementary information.     

Mitral valve prolapse in patients with coronary artery disease. Echocardiographic-angiographic correlation.

Echocardiography was performed in 25 consecutive patients with angina pectoris and angiographically demonstrable coronary artery disease. Left ventricular echograms detected late or pansystolic mitral valve bowing suggesting of mitral valve proplapse in 6/25 (24%). Left ventricular angiography showed prolapse of the posterior mitral leaflet in 15/25 (60%), including 5 detected by echocardiography. Significant triple vessel coronary disease was present in 11 of 15 patients with prolapsed mitralvalve. In each of the latter a greater than 90 per cent obstructive lesion was noted in at least one coronary artery: right coronary artery, 9 subjects (82%); left circumflex coronary artery, 5 patients (33%); and left anterior descending coronary artery, 4 patients (27%). Of 15 subjects with angiographic evidence of mitral valve prolapse, 13 had left ventricular asynergy-inferior or inferoposterior in 8 subjects (62%) and anterior or anteroapical in 5 subjects (38%). Eleven subjects had vectorcardiographic evidence of transmural myocardial infarction-inferior or inferoposterior in 9 (82%) and anteroseptal in 2 (18%). A single subject with mitral valve prolapse had mild mitral regurgitation. It is concluded that: (1) coexisting prolapse of the posterior mitral valve leaflet and coronary artery disease is usually associated with triple vessel obstructive lesions, (2) severe right coronary disease, inferior left ventricular wall asynergy, and inferior myocardial infarction are important angiographic and vectorcardiographic correlates, and (3) echocardiography will detect such mitral valve prolapse in only one-third of affected cases.     

Nocturnal angina in patients with fixed coronary stenosis. Increased coronary vasoconstrictive sensitivity with independence of pacing ischaemic threshold

Atrial pacing and ergonovine tests were performed in 18 consecutivepatients with unstable angina at rest and significant coronaryartery stenosis ( 90% in one vessel in 16 patients). 13 ofthem also had exertional angina. 14 patients presented at leastone positive response (1.0 mm ST-segment shift) to pacing, witha heart rate (144±11 vs 75±13 beats min^–1,P<0.001) and double product (195±26 vs 108±32x 10^–2 P<0.001) significantly higher than during anginaat rest. In the ten patients who presented nocturnal angina,the incidence of positive response to pacing and the pacingischaemic threshold, tested on three different days, were similarto those seen in the remaining patients. In contrast, the ergonovinetest was positive in all patients with nocturnal angina (100%),who required a low dose (0.28±0.2 mg), but it was positivein only four (50%) of those without nocturnal angina, who neededa higher dose (0.55±0.12 mg, P<0.005). Therefore, in patients with severe coronary stenosis and exertionalangina, spontaneous episodes, including nocturnal angina, arenot related to increases in heart rate. The increased coronaryvasoconstrictive sensitivity found in these patients, particularlythose with nocturnal angina, was not dependent on the statusof the coronary reserve, which strongly suggests that changesin coronary tone, focal or diffuse, are involved in the mechanismsof these ischaemic events.     

Mitral valve prolapse in coronary artery disease.

Mitral valve motion, left ventricular segmental contraction and severity of arterial stenosis were analyzed in 92 patients with coronary artery disease and 28 patients with "atypical chest pain" and normal coronary arterio-rams. Mitral valve motion was evaluated for the presence or absence of leaflet prolapse. Segmental contraction was evaluated by calculating the percent shortening of six chords of the left ventricle measured from right anterior oblique ventriculograms. The severity of disease in each coronary vessel (left anterior descending, left circumflex and right coronary) was graded on a scale of 1 (0 to 30 percent stenosis) to 5 (complete occlusion). Mitral valve prolapse was not suspected clinically but observed angiographically in 15 of 92 patients with coronary artery disease and in 5 of 28 patients with normal coronary arteriograms. In nine patients with coronary artery disease, the prolapse was restricted to the posterior leaflet, in five it was in both the anterior and the posterior leaflets and in one patient in the anterior leaflet only. Mitral regurgitation was noted in seven patients with coronary artery disease; it was mild in six and moderate in one. Among the patients with coronary artery disease, 12 of the 15 (80 percent) with mitral valve prolapse had left ventricular asynergy compared with 63 of the 77 (82 percent) without valve prolapse. The mean scores for severity of disease in the left anterior descending, circumflex and right coronary arteries were, respectively, 4.2, 2.5 and 3.2 in the patients with valve prolapse and 4.2, 2.2 and 3.5 in those without prolapse. In summary, there was no significant correlation between mitral valve prolapse and distribution of coronary arterial obstructions or abnormal patterns of left ventricular segmental contraction. There was a high frequency of mitral valve prolapse in patients with severe coronary artery disease and in those with normal coronary arteriograms and atypical chest pain.     

Colour Doppler echocardiographic assessment of regurgitant flow in mitral valve prolapse

Colour flow mapping was used to examine the pattern of regurgitantflow in 46 patients with mitral regurgitation due to mitralvalve prolapse. Valve morphology was assessed from the real-timetwo-dimensional image and the presence of mitral regurgitationwas determined from real time Doppler. On morphological criteria11 (24%) patients had isolated or predominant anterior leafletprolapse, 22 (48%) patients posterior and 13 (28%) patientsbi-leaflet prolapse. A single regurgitant jet was detected in43 patients (93%) and multiple jets in three (7%). The directionof the regurgitant jet was assessed in multiple views in twoorthogonal planes (antero-posterior and medial-lateral) definedin relation to the mitral valve leaflets. The regurgitant jetwas eccentric in the antero-posterior plane of the mitral leafletsin 40 of 45 (89%) cases and in the medial-lateral plane in 36of 40 (90%) cases. Posterior leaflet prolapse was usually associatedwith antero-medially directed jets, anterior leaflet prolapsewith postero-central or postero-lateral jets and bi-leafletprolapse with predominantly postero-medial jets. In a subgroupof patients with significant mitral regurgitation and an eccentricregurgitant jet, a ‘swirling’ effect was producedwith late systolic flow in the body of the left atrium towardthe mitral valve. Colour flow mapping in patients with mitral regurgitation dueto mitral valve prolapse demonstrated eccentric jets in mostpatients. The direction of regurgitant flow appeared to dependgreatly on the dynamic anatomy of the mitral valve leafletsduring systole. Although a single jet was detected in most patients,multiple jets did occur in a minority.     

Comparison between regional myocardial perfusion reserve and coronary flow reserve in the canine heart

Diameter stenosis and flow reserve are indices of morphologicaland functional severity of coronary artery stenosis. Flow reservecan be determined at coronary arterial or at myocardial level.In the presence of functional collateral circulation, coronaryflow reserve and myocardial perfusion reserve may differ. We studied coronary flow, coronary flow reserve and myocardialperfusion reserve in an open chest dog model with intact collateralcirculation, before and after induction of coronary artery stenosis.Coronary flow was determined with perivascular ultrasonic flowprobes and myocardial perfusion reserve from digital angiographicimages, in the stenotic as well as the adjacent non-stenoticcoronary arteries. Before induction of a stenosis, a significant correlation existedbetween coronary flow reserve and myocardial perfusion reserveof the left anterior descending (r=0.59; P<0.005) and theleft circumflex arteries (r=0.84, P<0.005). In stenotic arteries,coronary flow reserve and myocardial perfusion reserve decreasedsignificantly (P<0.005), but in the adjacent non-stenoticarteries coronary flow reserve was not affected Myocardial perfusionreserve in the non-stenotic adjacent left anterior descendingartery decreased significantly (P<0.05) and no correlationwas found between coronary flow reserve and myocardial perfusionreserve, whereas in the adjacent non-stenotic left circumflexartery there was no statistically significant decrease (4.1± 1.6 3.5 ± 1.4) but there was a good correlationbetween coronary flow reserve and myocardial perfusion reserve(r=0.85; P<0.005). This study demonstrates that, in the presence of a stenosisand functioning collateral circulation, coronary flow reserveis not a reliable predictor of myocardial perfusion reserve;both parameters provide mutually complementary information.     

Clinical utility of two-dimensional magnetic resonance angiography in detecting coronary artery disease

AIMS: The accuracy of magnetic resonance angiography in detectingproximal coronary artery stenoses is unclear. We postulatedthat fast magnetic resonance angiography is capable of (1) imagingproximal coronary arteries, and (2) detecting stenoses of 50%of their luminal diameter. METHODS AND RESULTS: Thirty-five patients, referred for analysis of angina pectoris,underwent both conventional angiography and magnetic resonanceangiography of coronary arteries. A fast k-space segmented gradient-echotechnique was used during breath-holds. Two observers, blindedto the results of conventional angiography, independently analysedthe magnetic resonance studies for (1) length of visualizedsegments, and (2) presence of signal voids indicative of stenoses.From 140 proximal arteries, 15 (11%) were excluded because ofincomplete imaging or degraded image quality. Mean length ofthe visualized segments was 9±4 mm for the left main,62±16 mm for the left anterior descending, 21±9mm for the left circumflex and 89±32 mm for the rightcoronary artery. Sensitivity for detecting 50% luminal diameterstenoses was 0·00 for the left circumflex, 0·53for the left anterior descending coronary artery, 0·71for the RCA and 1·00 for the left main artery. Specificityvaried from 0·73 for the left anterior descending coronaryartery to 0·96 for the left circumflex. Inter-observeragreement was 0·90. CONCLUSION: Thus, segmented magnetic resonance angiography is capable ofnon-invasive imaging of proximal coronary anatomy. Its goodaccuracy in detecting left main coronary artery disease, intermediateaccuracy in detecting right coronary artery and left anteriordescending coronary artery stenoses, and low accuracy in detectingleft circumflex lesions fit within a range of sensitivitiesand specificities found by others. Further technical advancesare necessary to make the technique clinically robust.     

Left ventricular function in mitral valve prolapse: Assessment with radionuclide cineangiography

Abnormalities of left ventricular contraction in patients with mitral valve prolapse have suggested a myocardial factor in this disease. To determine systolic left ventricular function in mitral valve prolapse, technetium-99m gated equilibrium radionuclide cineangiography was performed in 47 patients with this diagnosis. In 39 patients without mitral regurgitation the average ejection fraction was normal at rest (average [± standard error of the mean] 57 ± 3 percent, normal 57 ± 1 percent, difference not significant) and exceeded the lower limits of normal in all but 1 patient, whose ejection fraction was 41 percent. However, ejection fraction during maximal exercise was lower for the group of patients with mitral prolapse without mitral regurgitation than for normal subjects (average 64 ± 2 percent, normal 71 ± 2 percent, p < 0.005). In eight patients with mitral prolapse and mitral regurgitation, the average ejection fraction was normal at rest but was diminished with exercise in comparison with both normal subjects and patients with mitral valve prolapse without mitral regurgitation. Chest pain, arrhythmia and the pattern or extent of mitral valve prolapse on echocardlography were not independently associated with impaired left ventricular functional reserve. We conclude that, although many patients with mitral valve prolapse have normal left ventricular function, there is a subgroup without mitral regurgitation in whom diminished left ventricular functional reserve is suggestive of a cardiomyopathic process.     

Mitral valve prolapse in short-term experimental coronary occlusion: a possible mechanism of ischemic mitral regurgitation

Experimental coronary occlusions were carried out in 12 closed-chest dogs to investigate the functional anatomic characteristics of the mitral valve complex during acute myocardial ischemia. Two-dimensional echocardiography was used to assess left ventricular function, the mitral valve complex, and left atrial size. Presence of mitral regurgitation was assessed by left ventricular contrast echocardiography. Thirty-seven coronary occlusions of up to 10 min in duration were carried out in proximal or distal locations in the left anterior descending and the left circumflex coronary arteries. Mitral regurgitation, which was mild in severity as judged by a small rise in pulmonary artery wedge pressures, was observed in 15 of 37 brief coronary occlusion experiments. Mitral valve prolapse was noted in all 15 experiments, as well as in four additional studies in which mitral regurgitation was not seen. The development of experimental mitral valve prolapse was explained by measurements that demonstrated a relative displacement of the papillary muscle tips toward the mitral orifice. We conclude that mitral valve prolapse is a common sequela of short-term coronary occlusion and is often associated with mild mitral regurgitation. Relative displacement of ischemic papillary muscles toward the mitral orifice appears to be a likely mechanism of acute ischemic mitral valve prolapse.     

Coronary flow velocity dynamics in normal and diseased arteries

Distal coronary flow velocity measurements were previously limited to open heart or experimental procedures. Unlike previous Doppler catheter techniques, a Doppler angioplasty flow wire permits flow velocity measurements in both the proximal and distal segments of normal and diseased coronary arteries. In order to determine the potential clinical application of the Doppler flow wire, we performed baseline and hyperemia flow velocity measurements in proximal and distal segments of 20 angiographically normal arteries (right coronary = 8; left circumflex = 7; left anterior descending = 5) and 29 significantly stenosed arteries. All 3 normal coronary arteries had a diastolic-predominant pattern in both proximal and distal segments; the right coronary artery showed significantly toss diastolic predominance. The coronary vasodilator reserve was similar in all three normal coronary arteries, and in the proximal and distal arterial segments. Abnormal arteries had significantly tower coronary vasodilator reserve (normal vs abnormal, 2.3 ± 0.8/ 1.6 ± 0.7; p < 0.02). Normal arteries had preservation of velocity parameters in the distal segments; abnormal arteries had a significant decrease in distal velocity parameters. The proximal-to-distal velocity ratio was thus significantly higher in abnormal arteries (2.4 ± 0.7 vs 1.1 ± 0.2; p < 0.001). The coronary vasodilator reserve in proximal and distal arteries—in addition to the proximal to distal velocity ratio—may provide functional and hemodynamic data complementary to coronary angiography in the assessment of coronary artery stenosis.     

Aberrant right ventricular branch of right coronary artery with mitral valve prolapse

A 37-year-old man presented with a three-week history of chest pain. Transthoracic echocardiography demonstrated a mitral valve prolapse and mild mitral insufficiency. Coronary angiography showed normal left main, circumflex, left anterior descending and right coronary arteries; however, the right ventricular branch of the right coronary artery had a separate ostium. Concomitant congenital heart abnormalities have been observed with coronary artery anomalies. Primary congenital coronary and valvular anomalies may have genetic heredity. In the present case, mitral valve prolapse was accompanied by a right ventricular coronary artery origin anomaly which, to the best of our knowledge, is the first report in the literature in which both anomalies presented together.     

Prolapse of the mitral valve: clinical spectrum and coronary arterial distribution

Coronary angiograms were reviewed in 31 patients with idiopathic prolapse of the posterior mitral leaflet. There were 19 males and 12 females, ranging in age from 33 to 69. The coronary artery which supplied the posterior descending branch was designated as dominant. There were 27 dominant right coronary arteries and 4 dominant left coronary arteries. Attention was paid to whether the origin of the vessel which courses in the posterior atrioventricular groove branch was from the right coronary artery or the left circumflex. In the dominant right coronary artery group, the arterioventricular groove branch arose from the right coronary artery alone in 6 and from the left circumflex alone in 1 patient, and in 20 patients, from both. In the dominant left coronary artery group, the atrioventricular groove branch arose from the left coronary artery in all 4 patients. The frequency of dominant right coronary artery and left coronary and the origin of the atrioventricular groove branch did not differ in the patients with prolapse of the mitral valve from a control group of 30 patients similarly analyzed. In all instances, the atrioventricular groove branch arose from either the right coronary artery ro the left circumflex, or both. In no case was the arterioventricular groove branch totally absent. The results of this investigation do not support the thesis, previously advanced by others, that prolapse of the mitral valve is related to absence of the left circumflex coronary artery, but indicate a normal range of variation in coronary arterial distribution.     

Assessing coronary stenosis. Quantitative coronary angiography versus visual estimation from cine-film or pharmacological stress perfusion images

Visual judgment of stenosis severity from cine-film or single-photonemission computed tomographic dipyrida-mole perfusion imageswas compared to assessment of stenosis severity as measuredwith digital quantitative coronary angiography. Thirty patientswith angiographically verified single-vessel disease underwentdipyridamole thallium stress testing within 90 days of angiography. RESULTS: A percent diameter stenosis of 50%, a percent area stenosisof 75% and a stenotic flow reserve of <3·75 measuredby quantitative coronary angiography (CMS, version 1·1,Medis Inc.) corresponded to haemodynamically significant stenosisas evaluated by visual estimates from cine-film or perfusionimages. Quantitative coronary angiography percent diameter stenosis(51·2% ± 12·6%) correlated closely (r=0·74)but underestimated significantly visual assessment of stenosisseverity from cine-film (69·3% ±21·2% p=0·0001).However, quantitative coronary angiography percent area stenosis(74·7% ± 11·7%) more closely reflectedvisual estimates from cine-film (P=0·19). Quantitativecoronary angiography stenotic flow reserve showed the highestpositive and negative predictive value regarding visual estimatesfrom cine-film (88%, 86%) or perfusion images (88% 64%) followedby percent diameter stenosis (86% 75% 86% 56%) and percent areastenosis (87% 80% 87% 60%), respectively. CONCLUSION: Evaluation of coronary lesions by quantitative coronary angiographycorresponds closely with visual estimates from cine-film andhaemodynamic significance as evaluated by dipyridamole perfusionimages. (Eur Heart J 1996; 17: 1167–1174)     

Non-invasive evaluation of coronary reserve. Assessment of coronary reserve in patients with coronary artery disease by transesophageal-Doppler echocardiography

We assessed coronary flow reserve using transesophageal Doppler echocardiography in patients with coronary artery disease. The study included 33 coronary artery disease patients who were undergoing coronary arteriography. The blood flow velocities of the left anterior descending artery before and after intravenous infusion (0.56 mg/min for 4 min) of dipyridamole were recorded using transesophageal Doppler echocardiography. Fourteen normal healthy individuals, matched for age, served as a control group. The index of coronary flow reserve, i.e. the ratio of dipyridamole to baseline maximum diastolic velocity, was calculated. Maximal coronary flow reserve in coronary artery disease patients was significantly lower than in the control group (1.4+/-0.2 vs. 2.8+/-0.3, P<0.001). The coronary artery disease patients were classified into three groups: Group A included 10 patients with <50% left anterior descending artery stenosis; Group B included seven patients with 50-69% left anterior descending artery stenosis; 16 patients with >70% left anterior descending artery stenosis constituted Group C. The maximum coronary flow reserve was significantly different for A vs. B and A vs. C. (A, 1.77+/-0.18; B, 1.51+/-0.1; C, 1.28+/-0.24). A strong and significant correlation was found between the maximum coronary flow reserve and the degree of proximal left anterior descending artery stenosis (r=0.78, P<0.001). Coronary artery disease patients without left anterior descending artery stenosis on the arteriogram exhibited lower maximum coronary flow reserve compared to the control subjects (1.78+/-0.19 vs. 2.8+/-0.3, P=0.000).     

Dose-related effects of intracoronary nitroglycerin on coronary hyperemia in patients with coronary artery disease

Although intracoronary nitroglycerin (NTG) is frequently required during percutaneous transluminal coronary angioplasty or thrombolysis, the dose-related hemodynamic effects and the extent to which intracoronary NTG-induced coronary hyperemia is limited in patients with coronary artery disease have not been defined. Therefore, we studied 19 patients with coronary artery disease (nine with no or minimal luminal narrowing of the left anterior descending coronary artery [group 1] and 10 with significant left anterior descending coronary stenosis [group 2]); mean arterial pressure and thermodilution coronary sinus and great cardiac vein blood flow were measured during bolus administrations of 50, 200, and 300 μg of intracoronary NTG. During the NTG-induced hyperemia, mean arterial pressure decreased 0%, 4% (bothp =NS), and 6% (p < 0.05) after 50, 200, and 300 μg doses, respectively. Heart rate did not change. Global coronary hyperemia was greatest for 200 μg with coronary blood flow increasing (74 ± 32% in group 1 and 53 ± 25% for group 2) but was significantly different from 50 μg only in group 2 patients. Moreover, the regional coronary blood flow responses were attenuated in group 2 compared to group 1 for 50 μg, 18 ± 13% vs 38 ± 18%, and for 200 μg, 35 ± 15% vs 72 ± 34% (bothp < 0.05), with the reduction of regional coronary resistance in group 2 attenuated for all three doses of intracoronary NTG. The 300 μg dose did not provide further augmentation of either global or regional coronary blood flow or greater reduction in coronary resistance. We conclude that intracoronary NTG-induced hyperemia is, in part, dose related and attenuated in patients with severe coronary artery disease. These data reemphasize the reduction in coronary vasodilatory reserve in regions supplied by coronary arteries with severe stenoses. Moreover, during interventions requiring intracoronary NTG, doses above 200 μg do not appear to further augment coronary blood flow, probably because of NTG-induced systemic hemodynamic effects and coronary autoregulation.     

Failure to demonstrate myocardial ischaemia in patients with angina and normal coronary arteries. Evaluation by continuous coronary sinus pH monitoring and lactate metabolism

Visual judgment of stenosis severity from cine-film or single-photonemission computed tomographic dipyrida-mole perfusion imageswas compared to assessment of stenosis severity as measuredwith digital quantitative coronary angiography. Thirty patientswith angiographically verified single-vessel disease underwentdipyridamole thallium stress testing within 90 days of angiography. RESULTS: A percent diameter stenosis of 50%, a percent area stenosisof 75% and a stenotic flow reserve of <3·75 measuredby quantitative coronary angiography (CMS, version 1·1,Medis Inc.) corresponded to haemodynamically significant stenosisas evaluated by visual estimates from cine-film or perfusionimages. Quantitative coronary angiography percent diameter stenosis(51·2% ± 12.6%) correlated closely (r=0·74)but underestimated significantly visual assessment of stenosisseverity from cine-film (69·3% ±21·2% p=0·0001).However, quantitative coronary angiography percent area stenosis(74·7% ± 11·7%) more closely reflectedvisual estimates from cine-film (P=0·19). Quantitativecoronary angiography stenotic flow reserve showed the highestpositive and negative predictive value regarding visual estimatesfrom cine-film (88%, 86%) or perfusion images (88% 64%) followedby percent diameter stenosis (86% 75% 86% 56%) and percent areastenosis (87% 80% 87% 60%), respectively. CONCLUSION: Evaluation of coronary lesions by quantitative coronary angiographycorresponds closely with visual estimates from cine-film andhaemodynamic significance as evaluated by dipyridamole perfusionimages. (Eur Heart J 1996; 17: 1167–1174)