Magnitude of myocardial potassium changes during acute alterations in pacing frequency in the in situ pig heart

A transient loss of potassium from cardiac tissue during increments in stimulation frequency has been found in different isolated preparations, but there is no agreement as to the magnitude and time course of this loss. In the present study myocardial potassium balance was determined during changes in heart rate in pigs with an intact circulation. The left azygos vein, which drains into the coronary sinus in this species, was cannulated and a shuntline to the right atrium established. Coronary sinus blood was thus continuously drawn from the shunt by a pump, without admixture of systemic venous blood, and myocardial release and uptake of potassium were determined before, during, and after periods of pacing tachycardia. A transient mean(SEM) loss of potassium (13.0(5.6) mumol X 100 g-1 or about 0.25 mumol per beat change in heart rate) occurred during the first 90 s after increasing heart rate by a mean(SEM) of 53(4) beats X min-1. By discontinuing pacing heart rate returned to control values (mean(SEM) -43(7) beats X min-1), and myocardial potassium uptake ensued (mean(SEM) 9.8(3.3) mumol X 100 g-1 or 0.23 mumol per beat change in heart rate). The peak changes in coronary sinus potassium concentrations occurred 30 s after heart rate). The potassium lost during the periods of pacing tachycardia represented only about 0.2% of total myocardial potassium, equivalent to a reduction in intracellular potassium concentration of 0.3 mmol X litre-1. Since intracellular sodium and calcium concentrations are closely linked to the potassium concentration, the observed changes in potassium concentrations, although small, may be related to the positive inotropic effect of pacing tachycardia (the positive staircase phenomenon).     

Pacing and reperfusion induced arrhythmias: protection by slow heart rate in the rat heart

Using the isolated perfused rat heart with transient (10 min) regional ischaemia induced by coronary artery ligation, we have shown that slow heart rate can dramatically reduce the vulnerability of the myocardium to reperfusion induced ventricular fibrillation and ventricular tachycardia. In the heart rate range of 200-400 beats.min-1, slower heart rates exerted a frequency dependent protective effect against reperfusion induced arrhythmias. At the optimal rate of 200 beats.min-1, the incidence of total ventricular fibrillation (irreversible plus reversible) and ventricular tachycardia fell to 33% and 50% of their control values (100%). The anti-arrhythmic effect was achieved with only a minor (less than 20%) effect on coronary flow. To ascertain whether or not slow heart rate achieved an absolute reduction in vulnerability to arrhythmias irrespective of the duration of ischaemia, hearts were also subjected to 5, 10, 20, 30 or 40 min of ischaemia followed by 30 min of reperfusion with and without pacing at 200 beats.min-1. A bellshaped time-response profile was obtained in both groups. In unpaced controls (n = 12) this gave a maximal vulnerability to arrhythmias after 10 min of ischaemia. In the paced hearts (n = 12) the curve was shifted to the right, with a peak vulnerability at 20 min. These results show that the action of pacing is to exert a delaying effect which extends the duration of ischaemia that can be tolerated before the heart becomes vulnerable to reperfusion induced arrhythmias. Heart rate can have a substantial effect on reperfusion induced arrhythmias and should be considered when making therapeutic interventions and risk assessments in this setting.     

Potassium exchange in the human heart during atrial pacing and myocardial ischaemia

Potassium homoeostasis in the heart was studied during atrial pacing in 20 patients undergoing diagnostic coronary angiography. The potassium concentrations in the coronary sinus and a systemic artery were recorded continuously by means of catheter tip potassium electrodes. Ten patients with coronary artery disease and a positive exercise test developed chest pain and ST segment depression on the electrocardiogram during atrial pacing. Potassium concentrations in the coronary sinus rose initially and increased further when myocardial ischaemia developed. Ten patients including five with normal coronary arteries remained symptom free during atrial pacing with no electrocardiographic changes. In these patients coronary sinus potassium concentration increased at the onset of pacing, but returned to near control values despite continued pacing. In both groups arterial potassium concentration remained constant. Immediately after the end of pacing there was an abrupt transient fall in potassium concentrations in the coronary sinus to below control values. These results indicate that in man, as in other species, an increase in heart rate causes the transient movement of potassium out of the cell into the extracellular space. The onset of myocardial ischaemia is associated with a further loss of potassium from the cell. The end of pacing or ischaemia is accompanied by a re-uptake of potassium by heart muscle.     

Potassium exchange in the human heart during atrial pacing and myocardial ischaemia.

Potassium homoeostasis in the heart was studied during atrial pacing in 20 patients undergoing diagnostic coronary angiography. The potassium concentrations in the coronary sinus and a systemic artery were recorded continuously by means of catheter tip potassium electrodes. Ten patients with coronary artery disease and a positive exercise test developed chest pain and ST segment depression on the electrocardiogram during atrial pacing. Potassium concentrations in the coronary sinus rose initially and increased further when myocardial ischaemia developed. Ten patients including five with normal coronary arteries remained symptom free during atrial pacing with no electrocardiographic changes. In these patients coronary sinus potassium concentration increased at the onset of pacing, but returned to near control values despite continued pacing. In both groups arterial potassium concentration remained constant. Immediately after the end of pacing there was an abrupt transient fall in potassium concentrations in the coronary sinus to below control values. These results indicate that in man, as in other species, an increase in heart rate causes the transient movement of potassium out of the cell into the extracellular space. The onset of myocardial ischaemia is associated with a further loss of potassium from the cell. The end of pacing or ischaemia is accompanied by a re-uptake of potassium by heart muscle.     

Transient ischaemia induced by rapid cardiac pacing results in myocardial preconditioning.

STUDY OBJECTIVE--The aim was to determine whether rapid ventricular pacing can protect against the ventricular arrhythmias occurring during a subsequent coronary artery occlusion. DESIGN--The effect was examined of two 2 min periods of pacing (300 beats.min-1) in chloralose-urethane anaesthetised dogs on a subsequent 25 min coronary artery occlusion. Ventricular arrhythmias, ST segment elevation, and inhomogeneity of conduction were analysed. EXPERIMENTAL MATERIAL--25 anaesthetised mongrel dogs in a restricted body weight range were used. MEASUREMENTS AND MAIN RESULTS--Preocclusion pacing reduced the severity of occlusion induced ST segment elevation, degree of inhomogeneity, and arrhythmias: ventricular premature beats were reduced from 528(SEM 40) to 136(45), and there were lower incidences of ventricular fibrillation (0% v 47%) and ventricular tachycardia (30% v 80%). CONCLUSIONS--Rapid ventricular pacing "preconditions" the myocardium in a manner similar to that following short coronary artery occlusions. Short periods of ischaemia no matter how induced protect the heart against the arrhythmogenic effect of a prolonged coronary artery occlusion.     

Impaired coronary vasodilator responsiveness as a cause of lactate production during pacing-induced ischemia in patients with angina pectoris and normal coronary arteries

Subgroups of patients with angina pectoris and normal coronary arteries are known to have pacing-induced lactate production and, therefore, myocardial ischemia. To examine the mechanism of this pacing-induced ischemia, the effect of incremental atrial pacing on coronary blood flow and metabolism was studied in 27 patients with angina and normal coronary arteries. Seventeen patients continued to exhibit normal lactate extraction even at heart rates up to 160 beats/min (Group 1), whereas in 10 patients (Group 2) lactate extraction changed to production at the highest pacing rate. Coronary blood flow increased in Group 1 patients by 18, 41 and 75%, respectively, as heart rate was increased by 20 beat/min increments from 100 to 160 beats/min. In contrast, coronary blood flow increased by only 8, 7 and 14%, at the three respective pacing rates in Group 2. Between the heart rates of 100 and 160 beats/min, coronary vascular resistance decreased 32% in Group 1 patients but was unchanged in Group 2 patients. There was no significant change in the ratio of myocardial O2 consumption/rate-pressure product in Group 1 patients, but this ratio decreased from 0.91 +/- 0.26 ml O2 X min-1 X (mm Hg X beats/min)-1 to 0.53 +/- 0.11 (p less than 0.05) in Group 2 patients as heart rate increased from baseline to 160 beats/min. Thus, patients with angina and normal coronary arteries who develop ischemia with pacing have a decreased coronary vasodilator response that interferes with their ability to increase myocardial oxygen supply to match the higher demand.     

Influence of heart rate and atrial transport on left ventricular volume and function: relation to hemodynamic changes produced by supraventricular arrhythmia

The response of the left ventricle to pacing-induced changes in heart rate and the atrioventricular (A-V) relation was examined with equilibrium gated radionuclide ventriculography in 20 patients who had normal ventricular function after surgery for recurrent supraventricular tachycardia. In 10 patients count-derived left ventricular ejection fraction, end-diastolic volume and stroke volume were measured during sinus rhythm and during atrial pacing at 120, 140 and 160 beats/min. In the other 10 patients similar determinations were made during sequential A-V and simultaneous ventricular and atrial (V/A) pacing, both at rates of 100 and 160 beats/min. Left ventricular ejection fraction did not change significantly with atrial pacing (from 0.65 +/- 0.02 [mean +/- standard error of the mean] at a baseline sinus rate of 91 +/- 3 beats/min to 0.62 +/- 0.03 at 160 beats/min) despite a progressive decrease in end-diastolic volume. The percent reduction in end-diastolic volume (% delta EDV) and stroke volume (+ delta SV) from the baseline values was linear and related to change in heart rate (delta HR) as % delta EDV = -0.60 delta HR + 5.19 (r = 0.71; p less than 0.01) and % delta SV = -0.62 delta HR + 5.03 (r = 0.76; p less than 0.001). Left ventricular ejection fraction with baseline sequential A-V pacing at 100 beats/min was 0.67 +/- 0.03 and not significantly altered by either sequential A-V or simultaneous V/A pacing at 160 beats/min. At 100 beats/min, loss of atrial transport with simultaneous V/A pacing resulted in a small reduction in end-diastolic volume from a baseline value of -9.0 +/- 1.9 percent (p less than 0.01) and a nonsignificant reduction in stroke volume of -3.7 +/- 1.6 percent. During simultaneous V/A pacing at 160 beats/min, the reduction in end-diastolic and stroke volumes from the baseline value was -26.6 +/- 3.8 percent and -28.8 +/- 4.3 percent, respectively (both p less than 0.01), but was significantly smaller (-16.1 +/- 3.6 percent and -19.2 +/- 4.1 percent, respectively [p less than 0.05]) when atrial transport was maintained during sequential A-V pacing at the same heart rate. During simultaneous V/A pacing at 160 beats/min, two thirds of the reduction in end-diastolic and stroke volumes from the baseline value was due to the increment in heart rate as assessed from sequential A-V pacing and the other third was due to loss of atrial transport. The data indicate that the hemodynamic consequences of supraventricular tachyarrhythmias in patients with normal ventricular function are due primarily to decreases in ventricular volume as heart rate is increased and atrial contribution is lost rather than to any changes in left ventricular ejection fraction.     

Atrial rate-responsive pacing in sinus node disease

Patients with sinus node disease (SND) who are unable to achieve an adequate increase in heart rate during exercise are candidates for atrial rate-responsive pacing (AAI-R). We have implanted 40 AAI-R systems in SND patients with an average follow-up of 12.5 +/- 8 (range 3-30) months. All the patients received an activity-sensing pulse generator (Activitrax, Medtronic or Sensolog, Siemens-Pacesetter) with a single atrial lead. Only patients with an intraoperative AV nodal block cycle-length above 100 beats min-1 were included. During follow-up, one patient was observed to have transient asymptomatic 2:1 AV-block during sleep. No patient developed persistent AV-block or chronic atrial fibrillation. Twelve patients with persistent chronotropic incompetence were assigned for a randomized double-blind crossover study, comparing exercise treadmill capacity in AAI-R with conventional atrial inhibited pacing (AAI). During AAI-R pacing the maximum heart rate during exercise was 120 +/- 1 beats min-1 compared with 97 +/- 21 beats min-1 during AAI pacing (P less than 0.01). The average exercise time increased from 11.2 +/- 2 min during AAI-pacing to 13.4 +/- 3 min during AAI-R pacing (P less than 0.01). AAI pacing should be considered for patients with SND and chronotropic incompetence.     

Electrocardiographic correlates of myocardial ischaemia induced by atrial and ventricular pacing in dogs with coronary stenosis

We determined the electrocardiographic response to pacing-induced tachycardia in 45 dogs. Pacing was performed using left atrial, left atrial-right ventricular sequential or left atrial-left ventricular sequential modes at rates of 90 to 250 beats X min-1. Body surface isopotential maps in 15 dogs with normal coronary circulations defined the normal response to rate; surface potential extrema during the S-T segment increased in strength with increasing rate but spatial features remained constant. In the other 30 dogs, an ameroid constrictor was placed around the left circumflex coronary artery. Two weeks after implantation, atrial pacing to rates of 190 beats X min-1 or greater resulted in flat, S-T segment depression, with new and abnormal negative voltages registered over the inferior and left posterior torso. However, with either form of ventricular pacing, tachycardia with coronary obstruction did not alter the S-T segment response seen in control animals, in either intensity or spatial parameters. We interpret these findings to suggest that: in normal dogs, tachycardia produced a common electrocardiographic effect regardless of activation pattern; and tachycardia in the presence of coronary constriction results in subendocardial myocardial ischaemia that, with atrial pacing, reverses the normal transmural S-T segment potential gradient and causes body surface S-T segment depression, but with primary ventricular stimulation, the subendocardial ischaemia does not alter the transventricular repolarisation gradients sufficiently to generate body surface S-T segment shifts.     

Heart rate in humans during underwater swimming with and without breath-hold

Heart rate was monitored, by way of radiotelemetry, from 6 male subjects of mean age (+/- SE) 24 +/- 1 years and of mean mass 73.5 +/- 2.5 kg. Measurements were made in a 25 m pool at a water temperature of 28 degrees C. Resting heart rate was 67 +/- 3.7 beats X min-1 and when the subjects submerged themselves completely in the pool, but remained inactive, there was a prompt, gradual reduction in heart rate which reached 48 +/- 2.6 beats X min-1 within 30 sec and 40 +/- 2.6 beats X min-1 within 59 +/- 5.6 sec (maximum duration). When they propelled themselves under water for 33 sec by kicking their legs and breathed through a snorkel tube, heart rate increased progressively to a value of 118 +/- 4.1 beats X min-1 at 28 sec. However, when they performed the same manoeuvre while holding their breath, there was an initial increase in heart rate to 106 +/- 5.7 beats X min-1 within the first 10 sec. This was followed by a decline in heart rate which was more rapid than that recorded during inactive submersion and which eventually reached 48 +/- 4.4 beats X min-1 at mean underwater duration of 33 +/- 1.8 sec. It is concluded that during the first 10-15 sec of underwater breath-hold swimming in humans, the cardiovascular response (as indicated by heart rate) is similar to that seen during a similar level of exercise while breathing air. From then on there is a progressively more intense bradycardia which is probably indicative of an oxygen conserving response consisting of reduced perfusion of most of the body except the heart, CNS and active locomotory muscles. The degree and rate of onset of this proposed oxygen conserving response are influenced by the intensity of the exercise performed while under water and whether or not the period of underwater breath-hold swimming is preceded by exercise.     

Systolic time interval. Heart rate relationship during atrial or ventricular pacing

In order to evaluate the relative importance of heart rate (HR) and A-V synchrony during pacing, 16 patients with VVI pacemakers were compared with 8 patients with AAI pacemakers using systolic time intervals. The patients were examined at rest at increasing HR with increments of 10 beats/min until a maximum of 150 beats/min was reached or for AAI pacing until 2 degrees A-V block occurred. The slopes of the linear regression equations for PEP versus HR and PEP/LVET versus HR were used. To compensate for differences in baseline values, delta PEP% versus delta HR% and delta PEP/LVET% versus delta HR% were also calculated and used to evaluate the response to the two different pacing modes. PEP seemed in this situation to be less dependent on HR than expected from earlier data concerning spontaneous differences in heart rate. This is probably due to a lower catecholamine level during pacing. During AAI pacing the slopes were slightly more normal than during VVI pacing, but the differences did only reach statistical significance using PEP/LVET versus HR (p less than 0.05). At heart rates above 80 blood pressure had a tendency to be higher during AAI pacing, a trend which was only significant for the diastolic blood pressure at HR from 130-150. These results support the view, that the ability to increase heart rate is more crucial for left ventricular function than A-V synchrony in these patients.     

Bradycardia during severe but reversible hypovolemic shock in man

Severe bleeding and hypovolemic shock causing hypotension are most often associated with tachycardia. In response to passive head-up tilt, five healthy men exhibited an increase in heart rate (HR) from 62 to 79 beats X min-1 and a gradual increase in the plasma concentration of aldosterone and protein. The increase in HR was followed by a decrease of 29 beats X min-1 (range 11-46) at the time when blood pressure decreased 38 mmHg (6-73). When tilted back to 0 degree, blood pressure immediately reversed while HR remained unchanged. Hypotension was associated with large but variable increases in plasma vasopressin (86 +/- 28 pg X ml-1) accompanied by peripheral vasoconstriction. In two cases where patients with internal bleeding presented with a moderate HR of 96 beats X min-1, the ensuing fall in blood pressure was associated with a decrease in HR to 68 and 76 beats X min-1, respectively. Administration of albumin solution and blood normalized cardiovascular function. Two other patients showing initial HR of 130 and 100 beats X min-1, respectively, also developed relative bradycardia in conjunction with a decrease in blood pressure. Administration of ephedrine and atropine increased HR temporarily from 56 to 90 and from 36 to 110 beats X min-1, respectively. The latter two patients died in extreme bradycardia and autopsies revealed severe internal bleeding. It is concluded that although hypovolemic shock is most often associated with an increase in HR, the increase is modest and a paradoxical bradycardia develops in severe but potentially reversible hypotensive hypovolemic shock.     

Effects of inotropic and chronotropic stimuli on acute myocardial ischemic injury. III. Influence of basal heart rate

The influence of basal heart rate (HR) on the effects of inotropic (dobutamine infusion) and chronotropic (atrial pacing) stimuli during acute myocardial ischemia was assessed by measurement of intramural carbon dioxide partial pressure (PCO2) in open-chest dogs undergoing transient 10-minute left anterior descending coronary artery occlusions. In protocol I, in 5 dogs anesthetized with pentobarbital alone, HR increased from 153 +/- 10 to 182 +/- 7 beats/min between experimental coronary occlusions, but the increase in ischemic zone intramural carbon dioxide tension (delta PmCO2) was not altered by this significant increase in HR. In protocols II to V, dogs were anesthetized with combinations of morphine, thiamylal and pentobarbital and had a basal average HR of 81 beats/min. Atrial pacing in protocol II (13 dogs) increased HR from 76 +/- 21 to 134 +/- 19 beats/min (p less than 0.001); left ventricular (LV) myocardial oxygen consumption (MVO2) rose from 3.9 +/- 1.6 to 4.9 +/- 1.4 ml/min/100 g (p less than 0.05), and delta PmCO2 rose from 42 +/- 14 to 50 +/- 15 mm Hg (p less than 0.01), indicating more severe ischemic injury during the second experimental coronary occlusion. In protocol III, 11 dogs received 20 micrograms/kg/min of dobutamine before the second experimental occlusion, which significantly (p less than 0.02) increased HR, LV dP/dt and MVO2; delta PmCO2 increased from 46 +/- 13 to 63 +/- 18 mm Hg (p less than 0.01). The 7 dogs in protocol IV received 3.9 +/- 1.9 micrograms/kg/min of dobutamine, titrated such that HR was unchanged (84 +/- 10 vs 81 +/- 15 beats/min), but LV dP/dt increased by 92% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship between fluctuations in heart rate and asymptomatic nocturnal ischaemia

In order to quantify autonomic changes related to asymptomatic nocturnal myocardial ischaemia, we analyzed heart rate fluctuations recorded during Holter monitoring in 9 subjects with coronary heart disease (21 episodes) and in 11 age-matched controls. R-R interval spectral analysis was computed in sequences of 256 heart beats, taken during the ischaemic episode, 4, 8 and 60 minutes before, and 4 and 60 minutes after. Mean heart rate, R-R interval variability (assessed by R-R interval standard deviation), low and high (respiration-linked) frequency components of R-R interval spectrum were evaluated. Mean heart rate and R-R interval variability increased only during ischaemia (from 62.9 to 73.3 beats/minute, P less than 0.02, and from 39 to 88 msec, P less than 0.01, respectively). While high-frequency components of heart rate variability remained unchanged, low-frequency peak increased during ischaemia (from 9.4 to 43.3 sec2 X 10(-3)/Hz, P less than 0.01) and also 8 minutes (P less than 0.05) and 4 minutes before (P less than 0.05). Despite a moderate increase of heart rate occurring only during ischaemia, the early rearrangement of heart rate fluctuations suggests the occurrence of changes of autonomic tone before the electrocardiographic onset of ischaemia. Due to its limited amount, this phenomenon appears to be a consequence, most likely unspecific, of factors responsible for the genesis of myocardial ischaemia.     

Transmural coronary vasodilator reserve, and flow distribution during tachycardia in conscious young swine with right ventricular hypertrophy

Regional distribution of myocardial blood flow (MBF) was examined in eight normal and nine pulmonary artery banded (PAB) pigs before and during pacing induced tachycardia (heart rates: 175, 225 and 275 beats X min-1) as well as during iv adenosine infusion (1.5 mg X kg-1 X min-1; maximal coronary vasodilatation) using radionuclide labelled 15 micron diameter microspheres that were injected into the left atrium. It was observed that MBF per unit myocardial mass in the hypertrophied right ventricle (RV) of PAB pigs was similar to that in the RV of normal pigs. Also, minimal coronary vascular resistance per unit myocardial mass was similar between the two groups of pigs for RV as well as left ventricle (LV). This suggests that the increase in RV myocardial mass of young PAB swine was attended by appropriate adjustments in functional cross-sectional area of the RV coronary vascular bed. Despite similarity of maximal coronary vasodilator capacity in the two groups of swine, during pacing induced tachycardia MBF in the hypertrophied RV subendocardium as well as the right and middle layers of the interventricular septum in PAB pigs increased to a significantly lower level than in normal pigs and the RV endo:epi perfusion ratio, unlike in normal pigs, decreased to near unity. Increments in transmural LV MBF of PAB pigs were also attenuated during pacing at 225 and 275 beats X min-1 but the LV endo:epi perfusion ratio for the two groups of pigs remained similar. These findings suggest a possible overall depression of myocardial function in PAB swine.     

Changes in heart rate during obstructive sleep apnoea.

The mechanisms behind the decrease in heart rate during apnoeas in patients with obstructive sleep apnoea (OSA) are little known. Recent findings in animal experiments indicate that stimulation of the upper airway activates postinspiratory and cardiac vagal neurones in the medullary respiratory centre, causing alterations in heart rate and respiratory rhythm. Since OSA leads to a collapse of the airway and consequent stimulation of upper airway receptors, we studied the interrelations between heart rate and respiratory rhythm during apnoea and during negative intrathoracic pressure generated by the Mueller manoeuvre (MM). Fifteen patients with OSA (apnoea hypopnoea index (AHI) 45 +/- 28.h-1) were studied by polysomnography, during a MM and a Valsalva manoeuvre, each of 15 s duration. The heart rate decrease (delta HRA) and the increase in total respiratory cycle duration (TOT) were evaluated during apnoea in non-rapid eye movement (REM) sleep. Patients with OSA demonstrated a decrease in heart rate during apnoea (-14.4 +/- 9.0 beats.min-1), and during MM (-11.5 +/- 13.5 in OSA vs 3.1 +/- 7.8 beats.min-1 in a control group). TOT increased during apnoea (4.6 +/- 3.1 s). There was a significant correlation between delta HRA and AHI (r = -0.64) as well as between delta HRA and increase in TOT (r = 0.62). These findings indicate that upper airway obstruction may cause an activation of receptors at the site of airway collapse or distortion leading to changes in heart rate and respiratory rhythm.     

Hysteresis of the ventricular paced QT interval in response to abrupt changes in pacing rate

The rate of QT adaptation to abrupt changes in pacing rate was studied in seven patients with newly diagnosed complete heart block with a ventricular escape rate of less than 40 beats.min-1. Their median age was 70 (range 36-84) years, and none was taking any cardioactive medication known to affect the QT interval. From a baseline pacing rate of 50 or 110 beats.min-1 the ventricular rate was increased or decreased to a new level. The time taken for the ventricular paced QT interval to complete 90% of the change secondary to the change in rate was found to be 136(16) s (mean(SEM] when the rate was increasing and 189(25) s when the rate was decreasing (p less than 0.01). This time interval was independent of the magnitude of the rate change and the baseline heart rate from which the change occurred. Furthermore, the time course of QT adaptation was found to be exponential and was characterised by a time constant of 49.1(2.2) s when the rate was increasing and 60.4(2.0) s when the rate was decreasing (p less than 0.01). It is concluded that QT measurements in response to a change in pacing rate should take into account the time dependent nature of QT changes.     

Short-term effects of atrial versus atrio-ventricular pacing on myocardial ischaemia in coronary artery disease patients

This investigation was undertaken to evaluate the effects ofshort-term atrial vs atrio-ventricular pacing on myocardialischaemia. The study was in two parts. In part one, 12 coronary arterydisease patients were studied to investigate the effects ofthe two pacing modes on angina pectoris, coronary sinus O₂ saturationand lactate. The two pacing modes were each applied for 5 minat 25 beats. min^–1 more than the maximum heart rate ofthe exercise test. Coronary sinus O₂ saturation and lactatewere estimated before and after pacing. In part two, 13 patientswith left anterior descending coronary artery disease were studiedto investigate the effects of the two pacing modes on coronaryflow reserve, using a Doppler catheter in the above mentionedbranch after the administration of 10 mg intracoronary papaverine.The pacing rate was 15 beats . min^–1 greater than theresting heart rate. Coronary sinus lactate and O₂ saturation changes were the sameand angina pectoris developed at about the same time from thebeginning of pacing under both modes. Coronary flow reservewas 2.1±0.7 during atrial pacing and 2.1±1.1 duringatrio-ventricular pacing (ns). It is concluded that short-term atrial and atrio-ventricularpacing have the same effects on myocardial ischaemia in coronaryartery disease patients.     

Continuous recording of coronary sinus oxygen saturation during atrial pacing in patients with coronary artery disease or with syndrome X

Coronary sinus oxygen saturation was measured continuously during incremental atrial pacing in 34 patients undergoing cardiac catheterisation. In eleven patients with normal coronary arteriograms, negative exercise tests, and no ST segment depression on the electrocardiogram, an increase in the rate of atrial pacing transiently decreased coronary sinus oxygen saturation but within 20 s oxygen saturation returned to the control value. In six patients with coronary artery disease ST segment depression developed during atrial pacing. The coronary sinus oxygen saturation fell and remained reduced until pacing was discontinued. The size of the fall of coronary sinus oxygen saturation increased with increasing heart rate. In seven patients with coronary artery disease the ST segments were unaltered during atrial pacing and coronary sinus oxygen saturation did not fall. Ten patients with syndrome X were studied. In six ST segment depression developed on atrial pacing. In five, three of whom developed ST segment depression, the changes in coronary sinus oxygen saturation during atrial pacing were similar to those observed in patients without any evidence of coronary artery disease. In three, all of whom developed ST segment depression, coronary sinus oxygen saturation gradually increased throughout the period of atrial pacing. In two patients coronary sinus oxygen saturation fell in a manner similar to that observed in patients with obstructive coronary artery disease who developed ST segment depression on pacing. Thus regulation of coronary blood flow in normal persons in response to an increase of heart rate is rapid. Oxygen extraction across the coronary bed can increase by up to 30% and a persistent increase in oxygen extraction is an indicator of myocardial ischaemia. The term "syndrome X" does not describe a homogeneous group of patients but in the majority coronary sinus oxygen saturation does not fall despite symptoms and changes on the electrocardiogram, indicating that inadequate coronary blood flow is not the dominant mechanism.     

Continuous recording of coronary sinus oxygen saturation during atrial pacing in patients with coronary artery disease or with syndrome X.

Coronary sinus oxygen saturation was measured continuously during incremental atrial pacing in 34 patients undergoing cardiac catheterisation. In eleven patients with normal coronary arteriograms, negative exercise tests, and no ST segment depression on the electrocardiogram, an increase in the rate of atrial pacing transiently decreased coronary sinus oxygen saturation but within 20 s oxygen saturation returned to the control value. In six patients with coronary artery disease ST segment depression developed during atrial pacing. The coronary sinus oxygen saturation fell and remained reduced until pacing was discontinued. The size of the fall of coronary sinus oxygen saturation increased with increasing heart rate. In seven patients with coronary artery disease the ST segments were unaltered during atrial pacing and coronary sinus oxygen saturation did not fall. Ten patients with syndrome X were studied. In six ST segment depression developed on atrial pacing. In five, three of whom developed ST segment depression, the changes in coronary sinus oxygen saturation during atrial pacing were similar to those observed in patients without any evidence of coronary artery disease. In three, all of whom developed ST segment depression, coronary sinus oxygen saturation gradually increased throughout the period of atrial pacing. In two patients coronary sinus oxygen saturation fell in a manner similar to that observed in patients with obstructive coronary artery disease who developed ST segment depression on pacing. Thus regulation of coronary blood flow in normal persons in response to an increase of heart rate is rapid. Oxygen extraction across the coronary bed can increase by up to 30% and a persistent increase in oxygen extraction is an indicator of myocardial ischaemia. The term "syndrome X" does not describe a homogeneous group of patients but in the majority coronary sinus oxygen saturation does not fall despite symptoms and changes on the electrocardiogram, indicating that inadequate coronary blood flow is not the dominant mechanism.