CLINICAL STUDIES
Effects of pacing-induced and balloon coronary occlusion ischemia on left atrial function in patients with coronary artery disease
Christodoulos Stefanadis, MD, FESC, FACCa,
John Dernellis, MDa,
Eleftherios Tsiamis, MDa and
Pavlos Toutouzas, MD, FESC, FACCa
a Department of Cardiology, Hippokration Hospital, University of Athens, Athens, Greece
Manuscript received July 31, 1998;
revised manuscript received October 9, 1998,
accepted November 20, 1998.
Reprint requests and correspondence: Dr. Christodoulos Stefanadis, 9 Tepeleniou Str, 15452 Paleo Psychico, Athens, Greece
cstefan{at}atlas.voa.gr
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Abstract
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OBJECTIVES
The aim of this study was to compare left atrial (LA) function in 16 patients with distal left anterior descending (LAD) and in 16 patients with proximal left circumflex (LCx) coronary artery stenosis at rest and immediately after pacing-induced tachycardia (LAD-pacing [P] and LCx-P) or coronary occlusion (LAD-CO and LCx-CO).
BACKGROUND
During left ventricular (LV) ischemia, compensatory augmentation of LA contraction enhances LV filling and performance. The left atrium is supplied predominantly by branches arising from the LCx. Therefore, we hypothesized that one mechanism for the loss of atrial contraction may be ischemic LA dysfunction.
METHODS
Left ventricular and LA pressure–area relations were derived from simultaneous double-tip micromanometer pressure recordings and automatic boundary detection echocardiograms.
RESULTS
Immediately after pacing or after coronary occlusion, LV end-diastolic pressure, LV relaxation, LA mean pressure and LV stiffness significantly increased in all patients. However, the area of the A loop of the LA pressure–area relation, representing the LA pump function, significantly decreased in groups LCx-P and LCx-CO (from 14 ± 3 to 9 ± 2, and from 16 ± 4 to 9 ± 2 mm Hg·cm2, respectively, p < 0.05), whereas it increased in groups LAD-P and LAD-CO (from 12 ± 3 to 54 ± 10, and from 16 ± 3 to 49 ± 8 mm Hg·cm2, respectively, p < 0.001).
CONCLUSIONS
In patients with LAD stenosis, LV supply or demand ischemia is associated with enhanced LA pump function. However, in patients with proximal LCx stenosis who develop the same type and degree of ischemia, LA branches might have been affected, rendering the LA ischemic and unable to increase its booster pump function.
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Abbreviations and Acronyms
| | A | = area | | ABD | = automatic boundary detection | | CO | = coronary artery occlusion | | +dP/dt, –dP/dt | = positive and negative first derivative of pressure | | ECG | = electrocardiogram | | FAC | = fractional area change | | LA | = left atrial | | LAD | = left anterior descending | | LCx | = left circumflex | | LV | = left ventricular | | LVAed, LVAes | = left ventricular end-diastolic and end-systolic area | | P | = pacing | | ROI | = region of interest | | Tau | = time constant of relaxation |
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The left atrium is supplied predominantly by branches arising from the proximal left circumflex (LCx), with variable contributions from the right coronary artery (1–3). Therefore, proximal LCx coronary occlusions might be expected to compromise left atrial (LA) perfusion. Goldstein et al. (4) have reported the hemodynamic consequences of right atrial ischemia produced by dissection of all visible atrial coronary branches in a canine model. Furthermore, Berger et al. (5) investigated the mechanical effects of atrioventricular interaction and the role of atrial contraction during rapid atrial pacing in a hypertrophied canine model. No clinical study on LA function has been performed that shows abnormal LA function in patients with coronary artery disease. To assess the effects of ischemia on LA performance in the presence of left ventricular (LV) dysfunction due to ischemia, we studied the LA function during acute myocardial ischemia induced by rapid atrial pacing (P) and coronary artery occlusion (CO) in patients with distal single-vessel left anterior descending (LAD, groups LAD-P and LAD-CO) and in patients with single-vessel proximal LCx (groups LCx-P and LCx-CO) coronary artery stenosis.
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Methods
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Study population.
The study population consisted of 32 patients with coronary artery disease divided into four groups. Groups LAD-P and LAD-CO consisted of eight patients each (four men and four women) with mean age 48 ± 6 and 48 ± 7 years, respectively, with a significant ( 70% in diameter) coronary artery stenosis of the distal LAD (after the first diagonal branch). Groups LCx-P and LCx-CO consisted of eight patients each (four men and four women) with mean age 47 ± 6 and 48 ± 7 years, respectively, with a significant (70% in diameter) proximal stenosis of the LCx. Proximal LCx was  1 cm from the LCx origin measured in the left anterior oblique 40° with 30° caudal tilt or/and right anterior oblique 30° with 30° caudal tilt. Quantitative angiographic measurements were obtained using electronic digital calipers (DCI-S, Automated Coronary Analysis, Philips, The Netherlands). For each patient of the LCx-P and LCx-CO groups an age- and gender-matched patient was selected. All patients of groups LCx-P and LCx-CO had a LCx dominant coronary artery distribution. The class of angina pectoris according to the Canadian Cardiovascular Society (6) was comparable between patients of each group. All patients were in normal sinus rhythm, and none had a history of previous myocardial infarction, valvular disease, cardiomyopathy or any other concomitant heart disease. Rest LV ejection fraction on cineangiography was normal (55%) in all.
Ischemia was produced by rapid atrial pacing in patients of groups LAD-P and LCx-P and by CO at the site of the lesion during coronary angioplasty in patients of groups LAD-CO and LCx-CO. Furthermore, eight subjects with normal coronary arteries who were submitted to left heart catheterization for atypical chest pain were used as control subjects and undertook a pacing stress test protocol like patients of groups LAD-P and LCx-P. Informed consent was obtained from each patient and the study was approved by the ethical committee of our hospital. In all patients, medications except for sublingual nitroglycerin, which was allowed as clinically indicated, were discontinued five half-lives before the study. Left ventricular and LA cavity and walls were adequately visualized from conventional apical four-chamber echocardiographic views. This criterion was met in these 40 subjects after 43 subjects were initially screened. All patients were treated with aspirin, 325 mg orally, the day before the study and diazepam, 5 mg orally, 1 h before the procedure.
Left atrial function.
The LA pressure–area relation was calculated as previously reported (7,8) by retrograde nontransseptal access to the LA, which was achieved consistently and safely using a steerable LA catheter developed in our institution (for LA pressure measurements) (9–11) and automatic boundary detection (ABD) two-dimensional echocardiography (for simultaneous LA area measurements) (12,13).
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Retrograde LA catheterization
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All patients received 10,000 U of intravenous heparin before retrograde LA catheterization. A 7-F Millar double-tip micromanometer (Model 804-8169, pigtail), with the sensors 7 cm apart, was used for pressure measurements. Retrograde LA catheterization was performed according to our usual practice, as we have previously reported (7–11). A pacing wire was positioned in the high lateral right atrial wall for atrial pacing via a right femoral vein sheath (Fig. 1).
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Figure 1 Left lateral view of a radiographic image of the pigtail Millar catheter (which was inserted retrogradely) and the pacing wire. White arrows indicate the two tips of the micromanometers in the left atrium and left ventricle, respectively. Black arrow points to the tip of the pacing wire in the high lateral right atrial wall.
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Echocardiography.
All two-dimensional echocardiograms were performed with a Hewlett-Packard Sonos 2500 system equipped with a 2.5-MHz imaging transducer having an ABD application continuously before, during and after the tests. All ABD two-dimensional echocardiograms were obtained from the apical four-chamber view. Parasternal long-axis and short-axis views were obtained before the tests, every two min during pacing and after the completion of the ABD echocardiograms that were performed at the end of atrial pacing and of the balloon inflation, confirming the information obtained from the apical approach. Wall motion was qualitatively graded as normal, hypokinetic, akinetic or dyskinetic (14). In patients a wall motion score index was generated using 16 left ventricular wall segments at rest after rapid atrial pacing and after CO (15). Regional wall motion scores were determined from the review of the videotape by two expert observers.
Patients were placed in the supine position for simultaneous recordings of LA and LV area and atrial and ventricular pressures. First LA and then LV areas were recorded from the standard apical four-chamber view (7,8,12,13). To generate a region of interest (ROI) that accurately conforms to the blood pool, a circle or half-ellipse was positioned first around the left atrium and then around the left ventricle, respectively, and the system quickly and automatically generated an ROI. Then, we automatically proceeded to on-line graphical display of the instantaneous LA or LV area in cm2 (Fig. 2 and 3). Immediately after the cessation of pacing and before the balloon deflation, the two-dimensional ABD echocardiograms were recorded in the same sequence as baseline. Ischemic ABD echocardiograms were generally completed within 120 to 180 s after the termination of the test. Special efforts were made to take LA and LV areas from exactly the same position, using the same gain and compress during the echocardiographic procedure and from the same depth of the examination of the left atrium and the left ventricle with the prepacing baseline measurements. We have previously reported a very good reproducibility of this technique (7,8). All measurements were made at end-tidal volume apnea.
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Figure 2 Echocardiographic automatic boundary detection image (top) with the region of interest drawn around the left ventricle and the instantaneous cavity area displayed simultaneously with the electrocardiogram (ECG, bottom).
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Figure 3 Echocardiographic automatic boundary detection image (top) with the region of interest drawn around the left atrium and the instantaneous cavity area displayed simultaneously with the electrocardiogram (ECG, bottom).
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Study design.
Pacing stress test
Baseline measurements were obtained 30 min after the last infusion of contrast medium during a steady state period. A 12-lead electrocardiogram (ECG) was used for monitoring, and the ECG was regarded as positive for myocardial ischemia, if at least 1 mm or more of horizontal or down-sloping ST segment depression was produced. Right atrial pacing was initiated at a rate of 80 beats/min and was increased in a stepwise manner by 20 beats/min every two min. Ischemic end points of the pacing protocol were: pacing-induced angina, the presence of ischemic ST segment depression, the induction of segmental LV wall hypokinesia or dyskinesia or the rise in LV end-diastolic pressure greater than 5 mm Hg in comparison with the prepacing baseline.
Coronary angioplasty
The guiding catheter for the angioplasty procedure was advanced from the contralateral femoral artery, and coronary angioplasty was performed with routine techniques. Baseline measurements were obtained before placing the angioplasty balloon across the lesion during a steady state period. The second measurements were obtained just before the balloon deflation at the end of the first angioplasty balloon inflation of 60-s duration.
After cessation of the tests, echocardiographic imaging, ECG and pressures recordings were continued until the return of hemodynamic parameters and LV wall motion to the baseline state. Interpretable echocardiograms were obtained in all patients, and no patient was excluded because of a poor quality echocardiogram.
Analysis of data.
Hemodynamics were evaluated under steady state conditions by averaging three normal sinus beats in all of the analyses. Digitized signals were analyzed off-line by using the Microsoft 97 Excel for Windows computer program. The LA and LV pressure–area curves were obtained at baseline and immediately after the tests (Figs. 4 and 5).
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Figure 4 Representative left ventricular pressure–area loops, at baseline and immediately after pacing-induced ischemia from a patient with left anterior descending (LAD) coronary artery disease (A) and a patient with left circumflex (LCx) disease (B). An upward and rightward shift of the diastolic portion of the left ventricular pressure–area loop was observed as peak systolic pressure declined in both patients.
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Figure 5 Representative left atrial pressure–area loops, at baseline and immediately after pacing-induced ischemia from a patient with left anterior descending (LAD) coronary artery disease (A) and a patient with left circumflex (LCx) disease (B). An upward shift of the left atrial pressure–area loop was observed in the patient with LAD, whereas an upward and rightward shift of the left atrial pressure–area loop was observed in the patient with LCx. Furthermore, the area of the pressure–area A loop was significantly increased in the patient with LAD, whereas it decreased in the patient with LCx.
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There was a delay of the ABD image compared with the instantaneous invasive signal derived from the Millar catheter. This delay was dependent on the depth at which the echocardiographic study was performed and on the rate of sweep of the ABD image (7,8). To adjust for this delay, which varied among patients, the LV and LA area waveforms were confirmed with reference to a simultaneous ECG. Peak of the QRS complex of the digitized ECG was aligned to maximal LV ABD area and to minimal LA ABD area (16,17).
Left ventricular function.
Left ventricular areas were measured during the next 30 s after the LA area measurements. The following measurements and calculations were obtained: maximal positive and negative first derivative of LV pressure (peak +dP/dt and peak –dP/dt, respectively), LV minimal and end-diastolic pressure, peak systolic blood pressure, time constant of relaxation (Tau), LV stroke work index and LV stiffness constant. End-diastole was defined as the time that the LV dP/dt first exceeded 200 mm Hg/s. End-systole was defined as the point where the ratio between LV pressure and volume was maximal.
Left ventricular ejection indices
We measured LV end-systolic area (LVAes) and LV end-diastolic area (LVAed). The LV stroke area was calculated as LVAed – LVAes, and LV fractional area change as FAC = (LVAed – LVAes)/LVAes)/LVAed.
Left ventricular relaxation
Tau was calculated as previously described (7,8).
Left ventricular work index
Left ventricular stroke work index was calculated as the area of the pressure–area loop (Fig. 4).
Left ventricular stiffness
Left ventricular stiffness constant, ß, was determined by using the equation P =  eßA, where P = pressure (mm Hg), A = LV area (cm2), ß = area stiffness constant (cm–2) and = the factor characterizing the position of the pressure–area relation. Left ventricular pressure and area data derived from the minimal LV diastolic pressure to the peak of the A wave (18). Points less than a LV pressure of 5 mm Hg were excluded from analysis, because the LV diastolic pressure–area relation is not monoexponential at extremely low pressures and areas (19). This analysis integrates the viscous effects of early rapid filling and atrial contraction with passive chamber properties and, therefore, may not purely reflect passive chamber stiffness. In addition, it assumes a monoexponential relation between pressure and area that may not exist throughout the entire range of values studied. However, it provides a commonly used index of LV diastolic chamber stiffness (20).
Left atrial function.
Left atrial work indices
The areas of A loop and V loop were measured as previously described (Fig. 5) (7,8,21,22).
Left atrial area indices
Echocardiographic chamber areas were calculated by the digitized data. For each measurement, three separate beats were analyzed. The ABD-derived LA area at onset of LA systole measured at the peak of the P wave in the simultaneously recorded ECG (Aa) and end-systolic area (Amin) were used to compute LA systolic emptying index, which was defined as the ratio of (Aa – Amin)/Aa (7,8,12,13). Left atrial reservoir area was calculated from the difference between maximal LA area (Amax) minus Amin; LA conduit area was calculated from the difference between LV stroke area minus LA reservoir area.
Left atrial stiffness.
The passive elastic chamber stiffness constant a (in cm–2) was calculated as previously described (7,8).
Statistical analysis.
Repeated measures analysis of variance was used to detect statistically significant differences between the values of a continuous variable measured at two different times and between five independent groups. Thus, the model used included one within-subjects factor (time), one between-subjects factor (groups) and their interaction (groups by time). This full factorial model was developed to evaluate all possible main effects and interactions of the factors on the variable, which was under investigation each time. All tests were considered to be significant at a 0.05 level of statistical significance.
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Results
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All subjects had normal wall motion at rest. In groups LAD-P and LCx-P, the average heart rate increased to approximately 160 beats/min (range 140 to 180 beats/min). Angina pectoris developed in four patients of each group; ST segment depression was found in six patients of each group; hypokinesia of the LV wall was induced in all patients. In all 32 patients, the diameter of the LAD and LCx coronary artery at the point of their stenosis measured at baseline did not differ (LAD: 0.44 ± 0.14 and LCx: 0.45 ± 0.14 cm, p = NS). In each group of patients who underwent coronary angioplasty, five patients had chest pain, six patients had ischemic ST segment depression and segmental LV wall hypokinesia and rise in LV end-diastolic pressure greater than 5 mm Hg in comparison with the baseline was induced in all patients. Coronary angioplasty was successful in all 16 patients, with minimal residual coronary stenosis. Left ventricular and LA pressure and area measurements at baseline and after pacing or coronary occlusion in all groups are listed in Table 1. At baseline study, LV and LA dimensions and hemodynamics were similar with those of the normal subjects (p = NS).
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Table 1 Baseline and Pacing Stress Hemodynamics in Control Subjects, in Group LAD-P and in Group LCx-P and Baseline and Coronary Occlusion Hemodynamics of Group LAD-CO and Group LCx-CO
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Left ventricular alterations.
All subjects in the control group had normal wall motion after pacing, whereas all patients had wall motion abnormalities during the ischemic tests. Wall motion scoring index did not differ between groups after tests (p = NS, Table 2). Immediately after pacing and coronary occlusion, ischemic dilation of the left ventricle was noted in both groups of patients as both end-systolic and end-diastolic LV areas were increased (Table 1). Left ventricular stroke area significantly decreased in groups LCx-P and LAD-CO (p < 0.05), whereas it did not show significant decline in groups LAD-P and LCx-CO (p = NS). In all groups LV FAC was significantly decreased (Table 1).
Left ventricular maximal +dP/dt significantly decreased in all groups (Table 1). Peak systolic LV pressure decreased after pacing (group LAD-P: p < 0.05 and group LCx-P: p < 0.01), whereas it remained unchanged during coronary occlusion (group LAD-CO and LCx-CO: p = NS). Left ventricular stroke work index also decreased in all groups but reached a significant level in groups LAD-P and LCx-P (p < 0.05, Table 1). Moreover, pacing-induced ischemia resulted in depressed LV minimal –dP/dt, prolonged Tau, increased LV end-diastolic pressure (p < 0.001, for all comparisons) and increased LV stiffness (p < 0.001, for all comparisons, Table 1). There was an upward and rightward shift of the diastolic pressure–area curve during ischemia in all groups (Fig. 4). Changes of heart rate, diastolic blood pressure, LV end-diastolic area, stroke area and stroke work index that was observed after ischemia were similar in all groups (p = NS, Table 2), whereas changes of end-systolic area, systolic blood pressure, fractional area change (FAC), end-diastolic pressure, rate of LV pressure changes, Tau and stiffness constant were different between groups (Table 2).
Left atrial alterations.
Alterations were also observed in the LA function. Left atrial areas were increased in all groups after pacing stress or coronary occlusion, but these increases reached a significant level only in Amax, Aa and Amin in patients of group LCx-P (p < 0.05, p < 0.01 and p < 0.001, respectively) and of group LCx-CO (p = NS, p < 0.01 and p < 0.001, respectively). It was found that LA conduit area was significantly decreased in patients with LAD disease, whereas it was significantly increased in patients with LCx disease both after pacing and after coronary occlusion. Left atrial mean pressure had increased in all groups of patients (Table 1). Left atrial maximal +dP/dt significantly increased in groups LAD-P and LAD-CO (p < 0.001), whereas it significantly decreased in groups LCx-P (p < 0.001) and LCx-CO (p < 0.01, Table 1). Besides, LA A loop and systolic emptying index significantly increased in groups LAD-P and LAD-CO (p < 0.001, for all comparisons), whereas they were significantly decreased in groups LCx-P and LCx-CO (p < 0.05 and p < 0.001, respectively, for both groups). Left atrial stiffness also increased in groups LCx-P and LCx-CO (p < 0.001), whereas it did not change in groups LAD-P and LAD-CO (p = NS, Table 1). Although LA pressure during the V wave increased dramatically, there was a proportional increase in the X descent; thus, the stiffness constant that is derived from an exponential fit of the pressure–area data from the X to the V wave remained unchanged. In Table 2 we can see that all LA variables except for Amax were different between the five groups and after pacing or CO compared with baseline. Furthermore, the changes of these variables that were observed after pacing or CO were different between the five groups.
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Discussion
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The principal striking finding in the present study was the LA dysfunction during ischemia in patients with coronary heart disease. In this study, patients were specially selected so that investigation of the effects of rapid pacing or CO in the absence (patients with LAD stenosis) and the presence (patients with proximal LCx stenosis) of LA ischemia, when a comparable degree of LV ischemia was produced among groups, would be allowed. In patients with proximal LCx coronary artery stenosis, LA branches might have been affected, rendering the LA ischemic and unable to increase its booster pump function.
Ischemic LA dysfunction.
This study demonstrates that a consistent and predictable pattern of LA function abnormalities occurs during the induction of myocardial ischemia. We found that ischemia renders left atrium grossly dilated with depressed LA systolic function and alterations in LA diastolic stiffness. Venous return is inversely proportional to the instantaneous LA pressure, which is itself dependent on atrial stiffness and relaxation. Therefore, augmented LA contractility, by enhancing atrial relaxation, should facilitate atrial inflow. Conversely, depressed atrial performance impairs relaxation, an effect evident in the present study by the observed augmented X descent associated with LA ischemia. Furthermore, the increased loading conditions imposed on the left atrium by the stiff dilated left ventricle increase atrial oxygen demand at a time when the compressive effects of increased intracavitary pressure tend to diminish transmural perfusion, thereby increasing the ischemic burden on the thin-walled atrium (4).
It is interesting that the energy added by the left atrium to the blood (net atrial work) (23) was negative in patients with LCx (but not with LAD) disease during ischemia. This suggests that more energy is dissipated in the ischemic LA wall than can be added by the muscular contraction.
Contribution of LA function to LV performance.
Myocardial ischemia is known to cause myocardial dysfunction. It is known that for a similar amount of ischemia there is greater LV dysfunction in anterior compared with posterior ischemia (24). In the present study, although the amount of ischemia was similar between groups, its functional consequences were different. A possible explanation is that LV function during myocardial ischemia is not dependent only on the amount of the ischemia but also on the position in which ischemia is developed as well as on LV loading conditions, which in turn are in part dependent on LA transport function. However, LV preload during ischemia in patients with LCx disease and in patients with LAD disease was similar. Increased LA conduit function appeared to counterbalance the decreased LA systolic function. Perhaps the left atrium compensates for short periods of ischemia by shifting the contribution of its reservoir, conduit and booster functions; such compensation may ultimately fail, but convincing evidence after the ischemic insults in this study is lacking.
Our measurements have shown an inverse relation between LV and LA performance during LV ischemia in patients with LAD disease. Whereas LV stroke work index decreased, LA stroke work index increased significantly. The diminution of LV FAC was counterbalanced by an increased LA booster function; this increased function is clinically known as the "atrial kick" (25). Our results confirm the hemodynamic contributions of augmented atrial transport to performance of the ischemic left heart (25). Left ventricular dysfunction in the absence of atrial ischemia was associated with enhanced LA contraction, as indicated by more rapid A wave +dP/dt, increased peak A wave amplitude and augmented LA stroke work index. Left atrial mechanics appear similar to those of right atrial, wherein right ventricular dysfunction is accomplished with augmented right atrial contraction (4). Enhanced LA contractile function is probably a response to increased preload and afterload imposed by the stiff dilated left ventricle. In contrast, in patients with proximal LCx disease both left ventricle and left atrium suffered from ischemia during pacing-induced tachycardia or coronary occlusion. These results confirm previous findings reported by Sigwart et al. (25), who noted that LA function plays an important role in maintaining overall cardiac function during LV ischemia in patients with a significant stenosis of the LAD. In addition to these results we also found that in some patients with proximal significant stenosis of the LCx myocardial ischemia of the left atrium may result in dysfunction and loss of the atrial kick. These results are consistent with Hods’ findings (26) of acute LA ischemia as the pathophysiologic mechanism of early atrial fibrillation in acute myocardial infarction when there is occlusion of the LCx artery proximal to the origin of its LA circumflex branch.
Specific comments.
The LA branches were those branches that in the right anterior oblique 30° projection during prolonged recording were visible toward the atrioventricular groove, which was outlined by the coronary sinus. Another potential source of atrial blood supply is the sinus node branch, which arises from either the right or LCx with a distribution of approximately 55/45%, respectively. Whatever its origin, the artery usually branches around the superior vena cava base, commonly as an arterial loop from which small rami supply mainly the right atrium (1), and also the left atrium directly and/or by anastomoses with other LA branches (2,3). Unfortunately, convincing angiographic evidence that atrial blood supply was distal to the stenosis did not exist in patients with a LCx stenosis, because blood flow was decreased distal to the stenosis, making the small diameter atrial branches almost invisible on the angiography. On the other hand it must be noticed that there was no additional LA blood supply in these patients, as no LA branches were found originating from the right coronary artery. It is also possible that there was collateral blood flow through branches from the right coronary artery that prevented LA ischemia from occurring, which probably cannot be seen on angiography. Thus, the assumption that pacing or coronary occlusion in patients with a proximal LCx stenosis produces ischemia remains unproven. Nevertheless, the principal finding of this study regarding the differential effect of pacing or coronary occlusion on patients with a LCx stenosis in contrast with patients with an LAD stenosis remains immutable.
In the present study, the different degrees and types of LV dysfunction that have been obtained using different models of ischemia suggest that the ventricular response to ischemia should not be classified simply based on whether supply or demand ischemia is present but rather on a complex interaction between duration, extent, severity and type of ischemia elicited (27). Previous studies have shown that myocardial ischemia induced by coronary balloon angioplasty (28) or atrial pacing (29) results in a decrease in the LV inflow peak early to peak atrial velocity ratio. Other studies (30,31) have shown a proportionately greater increase in peak early velocity in patients with ischemia, which might reflect a higher initial pressure gradient during early diastolic filling compared with that of patients without ischemia. The reasons for these discrepancies between studies are not clear but may be related to the importance of LV preload on the pattern of LV filling (32).
The use of only the apical four-chamber view to evaluate LV and LA areas may have underestimated the severity of ischemic segments involving the inferior wall or the anterior wall, since the apical four-chamber view evaluates mainly the septum and lateral wall of the left ventricle. No mitral regurgitation was induced by pacing or coronary occlusion, at least at the time of evaluation of transmitral color flow imaging, which was applied after ABD application was finished. Nevertheless, we cannot exclude the occurrence of some mitral regurgitation during ischemia. Because hypokinesia (rather than dyskinesia) of the wall was induced at least in the adequately visualized segment, however, it seems unlikely that significant papillary muscle dysfunction occurred.
Clinical implications.
The magnitude of hemodynamic derangements associated with LV ischemia is determined to a substantial degree by the extent and severity of concomitant LA ischemic dysfunction. Thus, some patients develop life-threatening hemodynamic compromise despite a rather small extent of LV dysfunction. Our results demonstrated that when LV systolic function is depressed, LV performance is predominantly determined by the LA booster pump function (25,33). Compensatory augmentation of LA contraction enhances LV filling and performance, whereas loss of this function exacerbates conduit function. It appears that one important mechanism for the loss of this important enhancer of LV performance may be ischemic LA dysfunction.
Conclusions.
Ischemic LA dysfunction produces depression of LA booster pump function. This was associated with a significant increase in LA stiffness.
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Footnotes
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This study was supported by a grant from the Hellenic Heart Foundation.
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References
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|---|
- Gabella G. Cardiovascular system. Williams PL. Gray’s Anatomy. 38th ed. New York: Churchill Livingstone; 1995. p. 1507–1510
- James TN, Burch GE. The atrial coronary arteries in man. Circulation. 1958;17:90[Medline]
- James TN. Anatomy of the coronary arteries in health and disease. Circulation. 1965;32:1020[Abstract/Free Full Text]
- Goldstein JA, Tweddell JS, Barzilai B, et al. Right atrial ischemia exacerbates hemodynamic compromise associated with experimental right ventricular dysfunction. J Am Coll Cardiol. 1991;18:1564–1572[Abstract]
- Berger RD, Wolff MR, Anderson JH, Kass DA. Role of atrial contraction in diastolic pressure elevation induced by rapid pacing of hypertrophied canine ventricle. Circ Res. 1995;77:163–173[Abstract/Free Full Text]
- Campeau L. Grading angina pectoris. (letter)Circulation. 1976;54:522[Medline]
- Stefanadis C, Dernellis J, Stratos C, et al. Assessment of left atrial pressure-area relation in man using retrograde left atrial catheterization and echocardiographic automatic boundary detection: effects of dobutamine. J Am Coll Cardiol. 1998;31:426–436[Abstract/Free Full Text]
- Stefanadis C, Dernellis J, Stratos C, et al. Effects of balloon mitral valvuloplasty on left atrial function in mitral stenosis as assessed by pressure-area relation. J Am Coll Cardiol. 1998;32:159–168[Abstract/Free Full Text]
- Stefanadis C, Kourouklis C, Stratos C, et al. Retrograde left atrial catheterization with a new steerable cardiac catheter. Am Heart J. 1990;119:375–380[CrossRef][Medline]
- Stefanadis C, Kourouklis C, Stratos C, et al. Percutaneous balloon mitral valvuloplasty by retrograde left atrial catheterization. Am J Cardiol. 1990;65:650–654[CrossRef][Medline]
- Stefanadis C, Stratos C, Pitsavos C, et al. Retrograde nontransseptal balloon mitral valvuloplasty. Immediate results and long-term follow-up. Circulation. 1992;85:1760–1767[Abstract/Free Full Text]
- Waggoner AD, Barzilai B, Miller JG, Perez JE. On line assessment of left atrial area and function by echocardiographic automatic boundary detection. Circulation. 1993;88:1142–1149[Abstract/Free Full Text]
- Clarkson PBM, Wheeldon NM, Lim PO, et al. Left atrial size and function: assessment using echocardiographic automatic boundary detection. Br Heart J. 1995;74:664–670[Abstract/Free Full Text]
- Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two dimensional echocardiography. J Am Soc Echocardiogr. 1989;2:358–367[Medline]
- Presti CF, Gentile R, Armstrong WF, et al. Improvement in regional wall motion after percutaneous transluminal coronary angioplasty during acute myocardial infarction: utility of two-dimensional echocardiography. Am Heart J. 1988;115:1149–1155[CrossRef][Medline]
- Keren A, DeAnda A, Komeda M, et al. Pitfalls in creation of left atrial pressure-area relationships with automated boundary detection. J Am Soc Echocardiogr. 1995;8:669–678[CrossRef][Medline]
- Chen C-H, Nevo E, Fetics B, et al. Comparison of continuous left ventricular volumes by transthoracic two-dimensional digital echo quantification with simultaneous conductance catheter measurements in patients with cardiac diseases. Am J Cardiol. 1997;80:756–761[CrossRef][Medline]
- Gaasch WH, Cole JS, Quinones MA, Alexander JK. Dynamic determinants of left ventricular diastolic pressure-volume relations in man. Circulation. 1975;51:317–323[Abstract/Free Full Text]
- Glantz SA. Computing indices of diastolic stiffness has been counterproductive. Fed Proc. 1980;39:162–168[Medline]
- Applegate RJ. Load dependence of left ventricular diastolic pressure-volume relations during short-term coronary artery occlusion. Circulation. 1991;83:661–673[Abstract/Free Full Text]
- Hoit BD, Shao Y, Gabel M, Walsh RA. Left atrial mechanical and biochemical adaptation to pacing induced heart failure. Cardiovasc Res. 1995;29:469–474[CrossRef][Medline]
- Hoit BD, Shao Y, Gabel M, Walsh RA. In vivo assessment of left atrial contractile performance in normal and pathological conditions using a time-varying elastance model. Circulation. 1994;89:1829–1838[Abstract/Free Full Text]
- Grant C, Bunnell IL, Greene DG. The reservoir function of the left atrium during ventricular systole. An angiographic study of atrial stroke volume and work. Am J Med. 1964;37:36–43[CrossRef][Medline]
- Schneider RM, Morris KG, Chu A, et al. Relation between myocardial perfusion and left ventricular function following acute coronary occlusion: disproportionate effects of anterior vs. inferior ischemia. Circ Res. 1987;60:60–71[Abstract/Free Full Text]
- Sigwart U, Grbic M, Goy J, Kappenberger L. Left atrial function in acute transient left ventricular ischemia produced during percutaneous transluminal coronary angioplasty of the left anterior descending coronary artery. Am J Cardiol. 1990;65:282–286[CrossRef][Medline]
- Hod H, Lew AS, Keltai M, et al. Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion. Circulation. 1987;75:146–150[Abstract/Free Full Text]
- Applegate RJ, Walsh RA, O’Rourke RA. Comparative effects of pacing-induced and flow-limited ischemia on left ventricular function. Circulation. 1990;81:1380–1392[Abstract/Free Full Text]
- DeBruyne B, Lerch R, Meier B, et al. Doppler assessment of left ventricular diastolic filling during brief coronary occlusion. Am Heart J. 1989;117:629–635[CrossRef][Medline]
- Iliceto S, Amico A, Marangelli V, et al. Doppler echocardiographic evaluation of the effect of atrial pacing-induced ischemia on left ventricular filling in patients with coronary artery disease. J Am Coll Cardiol. 1988;11:953–961[Abstract]
- Presti CF, Walling AD, Montemayor I, et al. Influence of exercise-induced myocardial ischemia on the pattern of left ventricular diastolic filling: a Doppler echocardiographic study. J Am Coll Cardiol. 1991;18:75–82[Abstract]
- Carroll JD, Hess OM, Hirzel HO, Krayenbuehl HP. Dynamics of left ventricular filling at rest and during exercise. Circulation. 1983;68:59–67[Abstract/Free Full Text]
- Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic study. J Am Coll Cardiol. 1988;12:426–440[Abstract]
- Matsuda Y, Toma Y, Ogawa H, et al. Importance of left atrial function in patients with myocardial infarction. Circulation. 1983;67:566–571[Abstract/Free Full Text]
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