Sinus node deceleration during exercise as a marker of significant narrowing of the right coronary artery

Sinus Node Deceleration During Exercise as a Marker of Significant Narrowing of the Right Coronary Artery Todd D. Miller, MD, Raymond J. Gibbons, MD, Ray W. Squires, PhD, Thomas G. Allison, PhD, and Gerald T.’ Gau, MD variable, ranging from 6 to 35 beatslmin. Six patients had a 25 mm Hg decrease in systolic blood pressure compared with a measurement obtained at rest or an earlier stage of exercise. Figure I shows representative electrocardiographic tracings documenting a decrease in heart rate with continued exercise for all patients. Patients 3 and 4 had unique responses in the recovery period after exercise. Patient 3 had progressive sinus slowing, with eventual sinus arrest and a slow junctional escape rhythm of ~30 beatslmin. Patient 4 had progressive, marked sinus slowing to 35 beatslmin (Figure 2). Both patients had near syncope, with spontaneous resolution of symptoms, and increase in heart rate within I minute of lying in the supine position. Cardiac catheterization was pegormed within 6 months of the exercise study and interpreted according to Coronary Artery Surgery Study criteria.3 Results are listed in Table III. All patients had right dominant anatomy. All patients except patient 3 had 21 stenosis 290% in the right coronary artery; patients 2 and 7 had significant (290%) stenoses in the proximal segment of the vessel, whereas the other 4 had no stenosis >30% involving the proximal right coronary artery. Patient 3 had a maximal stenosis of 50% in the proximal segment

e hallmark of exercise-induced ischemia is ST-segr ment depression on the exercise electrocardiogram.

Other indicators of exercise-induced ischemia include ST-segment elevation, U-wave inversion, chronotropic incompetence, hypotension and ventricular ectopy. 1 Sinus node deceleration, defined as an initial increase and subsequent decrease in heart rate with continued exercise at the same or higher work load, has not been described as a marker of coronary artery disease. We previously reported a patient with sinus node deceleration and subsequent resolution on repeat exercise testing after angioplasty of a right coronary artery stenosis.2 In this study, we report an additional 7 patients with sinus node deceleration, all of whom had angiographically conGrmed disease of the right coronary artery. Clinical characteristics are listed in Table I. All patients except patient 4 were men. Table II lists the exercise test results. The maximal heart rates and blood pressures during exercise, and the subsequent lowest readings with continued exercise were recorded. The degree of sinus node deceleration during exercise was From the Department of Internal Medicine and Cardiovascular Discases, West 16-B, Mayo Clinic and Foundation, Rochester, Minnesota 55905. Manuscript received April 30, 1992; revised manuscript received and accepted August 10, 1992.

TABLE I Clinical Characteristics Pt. 1 2 3 4 5 6 7

A@ (year) 70 59 78 58 69 57 77

Prior MI

Priot PTCA

Inferior 0 Non-Q-wave Inferior 0 0 0

*Symptomsgraded B = p blocker; C = myocardial infarction; coronary artery; 1”AV

Medications

Symptoms*

+ (RCA) 0 0 + (RCA) + (RCA) 0 0

Atypical Angina Dyspnea Angina Angina Angina 0

N = long-acting

nitrate:

PTCA = percutaneous

Inferior LAD ST-T Inferior ST-T ST-T 1”AV

C, N N C, N C, N

B, C

according to New York Heart Association functional class I-IV. calcium antagonist: ECG = electrocardiogram: FC = functional = ftrst-degree atrioventricular

B, 0 B, B, B, 0

FC II FC IV FC Ill FC II FC II

ECG

transluminal

block; ST-T = nonspecific

class; LAD = left axis dewation: coronary

ST-T abnormality.

angioplasty;

MI

Ml

MI =

RCA = right

TABLE II Exercise Test Results Heart Pt.

Duration (min)*

1 2 3 4 5 6 7

7.3 (104) 8.5(101) 4.3 6.2 (112) 4.9 (68) 4.9 (56) 6.0 (97)

Angina 0 + 0 0 0 + 0

lschemic ECGt 0 + + + + + +

Thallium S inferior I inferior, S inferior, I inferior I inferior I inferior,

Images

lateral septal,

septal,

lateral

lateral

Rate (beats/min)

Rest

Highest

68 99 80 62 49 79 61

93 134 98 96 96 108 88

Blood

SubsequentS 67 127 63 82 90 89 80

Pressure

(mm Hg)

Rest

Highest

SubsequentS

110172

160170 174176 170182 120180 136/80

164178

155198

150/95

126172 176188 140/80 136176 145195 126170

134166

100/50 92150

‘All times Bruce protcco!, except patient 3 (Nau hton protocol). Numbers m parentheses are percentage of predicted time for age and sex. tDefined as t 1 m m horuontal or downsloping f T-segment depression 80 ms after J point. $Highest refers to highest recorded heart rate or blood pressure measurement durmg exercise. Subsequent refers to respective measurement at later time point during continued exercise at either same or higher work load. For patients 1,3 and 4, highest blood pressure measurement durmg exercise was recorded at peak exercise. ECG = electrocardiogram; I = ischemia; S = scar.

BRIEFREPORTS 371

TABLE III Cardiac Catheterization Results

Pt.

Left Ventricular Ejection Fraction (%)*

1 2 3 4 5 6

67 35 73 80 47

7

76

Regional Hypoklnesia* inferior Anterior, Inferior Inferior, lateral Inferior Septal Anterior, septal, Inferior, lateral Anterior

*For patients 3 and 4, left ventricular radionuclide anglography, respectively,

patient 2.

Percent Diameter Reduction of Coronary Arteryt

Lefl Ventricular End-Diastolic Pressure (mm Hg)

LM

LAD

LC

Right

28 20

0 0 0 0 40 30

60 40 90 20 40 70

20 100 99 50 0 80

100 100 50 100 90 100

9

40

90

90

90

24 -

ejectIon fracbon and regional hypakinesia were obtained by echocardiography rather than left ventriculography. Left ventricular ejection fraction not awlable

and for

tNumben listed are percent maximal stenoses for each coronary artery or its major branches. LAD = left anterior descending: LC = left circumflex; LM = left main coronary artery. J

of the right coronary artery. This vessel also hod aneurysmaldilatation and multiple 40% stenosesin distal segments.At the time of subsequentbypass surgery, jlow in the bypassgraft measuredonly 60 mllmin, providing further evidence that this vesselwas d$%sely diseaseddespite only a moximul stenosisof 50%. All patients except patient 5 had 21 stenosis250% in another coronary artery.

Sinus node deceleration appears to be a marker of severe atherosclerotic disease involving the right coronary artery. Six of these 7 patients, as well as the patient we previously reported? also had traditional ST-

cise bration (Arabic numeds showing minutes and see cds). All pathnts exercised acciwhg to Bruce protocol, except patient 3 (-on protocol). 372

THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 71

segment depression during exercise. Unlike ST-segment depression, which does not accurately localize the site of myocardial ischemia, sinus node deceleration identifies patients with inferior wall ischemia. The concept that inferior wall ischemia is the critical factor responsible for this phenomenon is supported by the following: (1) The stenoses in arteries other than the right coronary artery in patients 1,4 and 5 were only modest (20 to 60%) in severity. (2) Of 6 patients with thallium images, 3 had perfusion defects confined to the inferior wall. (3) The patient we previously reported2 had no significant &noses in the left-sided coronary arteries and a normal increase in heart rate during repeat exercise testing after successful right coronary artery angioplasty. The exact prevalence of sinus node deceleration is unknown, but appears to be very low. In the past 4 years, we have observed only 1 patient, other than in this study, with a decrease in exercise heart rate in a practice where approximately 10,000 exercise tests are performed annually. This patient did not undergo angiography, but had history of inferior wall myocardial infarction. Sinus node deceleration should be distinguished from “chronotropic incompetence,” a term popularized by Chin et al4 to describe a less than normal increase (but not a decrease) in heart rate during progressive exercise in patients not receiving p blockers. Five patients in this Patient

3

Patient

4

bmdyeMbforpatiemt4.lracimgforpatient3isl8adv~anduloseforpatientI-*leadsII(kft; md VI5 m9mFEBRUARY1,1993

study were receiving p blockers. Most patients (62%) with severe chronotropic incompetence have 3-vessel disease (250% stenoses in 3 coronary arteries).4 Including our previously reported patient,2 only 3 of 8 (38%) with sinus node deceleration had 250% stenoses in all 3 coronary artery distributions. Furthermore, exercise-induced hypotension does not occur with chronotropic incompetence,4 but did occur in 6 patients in this study. Patients with sinus node dysfunction also have a blunted increase in heart rate during exercise,5 but an initial increase followed by a decrease has not been described. The most likely mechanism to explain sinus deceleration is exercise-induced provocation of the Bezold-Jarish reflex. This reflex describes the vasodilation, bradycardia and hypotension that result from stimulation of inhibitory cardiac receptors located primarily in the inferoposterior wall of the left ventricle.6~7 Direct ischemia of the sinoatrial node causing sinus deceleration is unlikely, because only 2 patients had a high-grade stenosis in the proximal segment of the right coronary artery. The Bezold-Jarish reflex has been reported to occur during inferoposterior myocardial infarction, infe-

rior ischemia due to Prinzmetal’s angina, reperfusion of the right coronary artery, coronary angioplasty and exertional syncope in aortic stenosis.6,7 It was not previously described as occurring during exercise in patients with significant atherosclerotic disease of the right coronary artery. REFERENCES 1. Schlant RC, Froelicher VF Jr, Blomqvist CC, Hall RJ, Brandenburg RO, McCallister BD, DeBusk R, McHemy PL, Ellestad MH, Ryan TJ, Fletcher GF, Sheffield LT. Fisch C, DeSanctis RW, Dodge HT, Reeves TJ, Weinberg SL. Guidelines for exercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Assessment of Cardiovascular Rocedures (Subcommittee on Exercise Testing) J Am Coil Cardiol 1986;8:725-738. 2. Miller TD, Gibbons RJ. Pandoxic heart rate deceleration during exercise: relationship to a mid-right coronary artery stenosis. Chest 1988:94:407-40X. 3. Principal Investigators of CASS and their Associates. National Heart, Lung, and Blood Institute Coronary Artery Surgery Study. Circulahm 1981;63(suppl I): I-l-I-39. 4. Chii CF, Messenger JC, Greenberg PS, Ellestad MH. Chronotropic incompetence in exercise testing. Ch Cardiol 1979;2: 12-18. 5. Abbott JA, Hinchfeld DS, Ku&l FW, Scheinman MM. Graded exercise testing in patients with sinus node dysfunction. Am J Med 1977;62:33@338. 6. James TN. Cardiac innervation: anatomic and ohamacoloeic relations. BUN N Y Acad Med 1967;43:104-1086. 7. Mark AL. The Bezold-Jarish reflex revisited: clinical implications of inhibitory reflexes originating in the heart. J Am CON Cardiol 1983;1%0-102

BRIEF REPORTS 373