Influence of extra corporeal circulation on myocardial oxygen tension: results of an animal model

BACKGROUND: Experimental data have shown the potential risk of cellular damage of the myocardium during extra corporeal circulation (ECC). The influence of ECC on myocardial oxygen tension however remained unclear. Therefore, the influence of ECC on the oxygen tension in a beating heart was investigated. METHODS: In a pig animal model flexible pO2 microcatheters were positioned in the midmyocardium of the left ventricle and the skeletal muscle and tissue oxygen tension during ECC were monitored and compared with data of a control group without ECC. RESULTS: ECC and unload of the heart caused a significantly higher increase of myocardial pO2 than in a non-ECC control group. CONCLUSION: Our findings show the beneficial effect of ECC on myocardial pO2. This may support the use of ECC in coronary artery bypass grafting because the potential myocardial injury due to ECC is not related to myocardial ischemia. On the contrary, myocardial pO2 was even increased during extracorporeal circulation in this study.     

Cardiac adenosine production is linked to myocardial pO2

Experiments were performed on isolated perfused guinea-pig hearts (n = 45) to further evaluate the stimulus that triggers cardiac adenosine production. Stimulation of hearts with isoproterenol (4 nM, 20 min) enhanced left ventricular dP/dtmax, heart rate and myocardial oxygen consumption within 1 min to new steady state values, whereas coronary venous adenosine concentration only transiently increased reaching its maximum between 1 and 3 min of stimulation. Rate of accumulation of S-adenosylhomocysteine (SAH), a measure of the free cytosolic adenosine concentration, was steepest immediately following onset of stimulation and then progressively declined. Similar to adenosine, changes in coronary venous pO2 were phasic and adenosine release and pO2 closely correlated. Norepinephrine (20 nM) which increased myocardial oxygen consumption to a comparable extent as isoproterenol (4 nM) further decreased coronary venous pO2 and increased coronary venous adenosine. When myocardial oxygen supply was systematically varied by changing coronary perfusion pressure from 60 to 90 and 35 cmH2O, respectively, the adenosine release during isoproterenol (2 nM) was markedly enhanced at 35 cmH2O but blunted at 90 cmH2O. Similarly SAH accumulation was greatest at 35 cmH2O and smallest at 90 cmH2O. It is concluded that changing myocardial oxygen consumption is not a sufficient cause to enhance adenosine formation. Myocardial oxygenation as reflected by changes in coronary venous pO2 closely correlates with changes in free cardiac adenosine as evidenced by two independent indices: tissues SAH and coronary venous adenosine concentration. The stimulus triggering cardiac adenosine formation is most likely the imbalance of oxygen supply and oxygen demand.     

Myocardial oxygen tension determines the degree and pressure range of coronary autoregulation

Experiments were designed to separate effects of myocardial oxygen tension and oxygen consumption on coronary autoregulation. The approach was to measure coronary hemodynamic and metabolic responses to decreases in perfusion pressure during interventions that altered the balance between myocardial oxygen supply and demand. Studies were conducted in anesthetized heart-blocked dogs with the left coronary artery perfused from a pressure-controlled blood reservoir. Decreasing oxygen consumption by lowering heart rate from 120 to 40 bpm increased coronary venous oxygen tension and reduced the degree of flow autoregulation between 120 and 80 mm Hg by threefold. In contrast to effects of bradycardia, coronary constriction with vasopressin or indomethacin (heart rate 120 bpm), which produced comparable increases in baseline vascular resistance, decreased coronary venous oxygen tension, and augmented flow autoregulation by nearly twofold. Initial coronary venous oxygen tension but not oxygen consumption was strongly correlated with a quantitative index of autoregulation (-0.052 PO2 + 2.01, R2 = 0.86) over the pressure range of 120 to 80 mm Hg. When heart rate was lowered to 40 bpm and coronary venous oxygen tension subsequently reduced with vasopressin to control values (120 bpm), autoregulation was completely restored. Parallel studies examined the effects of metabolic and pharmacologic interventions on coronary pressure-flow relations over a wide range of pressures. For each 20 mm Hg decrement in pressure between 160 and 80 mm Hg, lowering heart rate attenuated autoregulation whereas pharmacologic coronary constriction augmented autoregulation. The observed variations in the autoregulation index were largely explained by differences in the prevailing venous oxygen tension. Furthermore, the upper pressure limit for autoregulation was dependent on venous oxygen tension with a threshold oxygen tension for autoregulation of 32 mm Hg. These results indicate that coronary autoregulation is closely coupled to the prevailing venous oxygen tension but not oxygen consumption and is facilitated at low venous oxygen tension.     

Delayed adaptation of ventricular repolarization after sudden changes in heart rate due to conversion of atrial fibrillation. A potential risk factor for proarrhythmia?

AIMS: Onset and termination of atrial fibrillation are often associated with abrupt changes in heart rate. Presence and time-course of delayed adaptation of the QT/QTc interval are unknown, but a temporary "mismatch" between rate and the QT interval may enhance the risk of proarrhythmia. METHODS: In a prospective two-part study, time-course of adaptation of ventricular repolarization after abrupt changes in heart rate was assessed during termination of Holter ECG-documented atrial fibrillation episodes (Group 1, 32 patients) and subsequently in 20 patients with sick sinus syndrome and cardiac pacing initiating abrupt bi-directional changes in paced heart rate (Group 2). RESULTS: Conversion of atrial fibrillation showed a 32+/-21 bpm fall in heart rate (P<0.05). Restoration of the QTc interval afterwards was delayed by < or =1 min in 27%, by 1-2 min in 21%, by 2-5 min in 11% and by >5 min in 41% of the cases. Atrial pacing simulating a 30 bpm fall/increase in atrial rate demonstrated that a subsequent transient rate-QT mismatch is a physiological phenomenon (fall of 100 to 70 bpm: initially 90% of the proper QTc interval, compared with 94% after conversion of atrial fibrillation). The restoration curve of QTc adaptation showed an initially fast and subsequently slower time component, with interindividual variation. Clinical parameters, baseline heart rate or the direction of rate changes were not predictive. CONCLUSION: Delayed adaptation of ventricular repolarization following atrial fibrillation onset and termination is common, requiring minutes for restoring the QT/QTc steady state. Clinical parameters fail to predict patients with a long-lasting rate-QT mismatch. It may carry a significant arrhythmogenic risk particularly in patients on QT altering medication.     

Exercise heart rate acceleration patterns during atrial fibrillation and sinus rhythm

Background: Patients with atrial fibrillation sustain a significant lower exercise tolerance compared to those in sinus rhythm, even while seemingly in adequate rate‐control. Methods: Exercise testing was performed during atrial fibrillation and after electric cardioversion for 30 patients who were initially treated with AV modifying agents and were considered in adequate rate control. Heart rate parameters were obtained during all exercise stages, and a graphic display of heart rate acceleration was obtained. For those patients who remained in sinus rhythm, an additional exercise test was performed after 1 month. Results: During atrial fibrillation, heart rate at the completion of Bruce stage 1 and the peak exercise heart rate were significantly higher when compared to sinus rhythm (120 ± 10 bpm vs. 98 ± 11 bpm and 164 ± 16 bpm vs. 129 ± 11 bpm respectively, p < 0.001 for both). The time to peak exercise heart rate was significantly shorter during atrial fibrillation (3.5 ± 1 min vs. 6.5 ± 1.5 min, p < 0.001), and the total exercise duration was subsequently shorter as well (6 ± 2 min vs. 8.5 ± 2 min, p < 0.001). Treatment with beta‐blockers prior to exercise did not affect the earlier peaking of the heart rate. After 1 month, similar time to peak heart rate and similar exercise performance were observed among patients, who remained in sinus rhythm, when compared to to the post‐cardioversion exercise test. Conclusions: In patients with atrial fibrillation, exercise heart rate acceleration displays a specific pattern of early peaking. Earlier heart rate peaking occurs regardless of ample rate control while at rest or mild physical activity and contributes to overall lower exercise performance. Ann Noninvasive Electrocardiol 2011;16(4):357–364     

Improved myocardial oxygen utilization by diltiazem in patients

Calcium entry blocking drugs produce different effects on systemic and coronary hemodynamics and myocardial oxygen extraction. To examine the effects on myocardial oxygen extraction, intravenous diltiazem (100 micrograms/kg bolus with a continuous 10 micrograms/kg/min infusion) was administered to 11 patients at rest and during controlled heart rates (100 +/- 5 and 120 +/- 5 bpm). At rest, diltiazem decreased mean arterial pressure from 109 +/- 13 to 99 +/- 14 mm Hg (p less than 0.01), increased heart rate from 64 + 12 to 74 +/- 14 bpm (p less than 0.01), and decreased coronary sinus resistance (1.02 +/- .41 to 0.87 +/- .40 U, p less than 0.05). Myocardial oxygen extraction was significantly reduced since coronary sinus oxygen content increased (6.0 +/- 0.9 to 7.8 +/- 1.2 ml/dl, p less than 0.01) and the arterial-coronary sinus oxygen difference decreased (12.0 +/- 1.7 to 10.6 +/- 1.6 ml/dl, p less than 0.01). Similar changes occurred with heart rate held constant. There were no significant changes in absolute coronary sinus blood flow, calculated myocardial oxygen consumption, or left ventricular dP/dt. Diltiazem decreases mean arterial pressure while reducing both myocardial oxygen extraction and coronary arterial resistance, suggesting that a principal mechanism of a beneficial effect upon the coronary circulation appears to be an improvement in myocardial oxygen extraction relative to myocardial oxygen demand.     

Cardioprotective effects of lowering oxygen tension after aortic unclamping on cardiopulmonary bypass during coronary artery bypass grafting.

The effect on myocardial reperfusion injury of reducing oxygen tension during reperfusion on cardiopulmonary bypass (CPB) in coronary artery bypass grafting (CABG) was examined at the same time as the influence of diltiazem during CPB was evaluated. A prospective, randomized trial evaluated the hemodynamic and myocardial metabolic recovery in 3 groups of patients undergoing elective CABG; subjects were randomly allocated on the basis of oxygen tension during reperfusion after aortic unclamping: group 1 (n=10) hyperoxic reperfusion (oxygen tension [PO2]=450-550 mmHg); group 2 (n=10): hyperoxic reperfusion and subsequent continuous infusion of diltiazem (0.5 microg/kg); group 3 (n=10): lowering reperfusate PO2 (PO2=200-250 mmHg). Hemodynamic and myocardial metabolic measurements were taken at 6 preset times: before starting the surgical procedure and at 30 min and 3, 9, 21, and 45 h after discontinuation of CPB. The cardiac index in the lowering reperfusate PO2 group was higher than that of the hyperoxic reperfusion groups at 30 min and 3 h after CPB, and malondialdehyde and troponin-T were significantly lower at 30 min and 3 h, respectively. In comparison with the hyperoxic + diltiazem group, the hemodynamic and myocardial recovery in the lowering reperfusate PO2 group was improved for about 3 h after CPB. Reduced oxygen tension during reperfusion after aortic unclamping on CPB is more effective against myocardial injury than a calcium antagonist in the short term. It is a convenient and safe management technique that can reduce morbidity and mortality, especially in the severely compromised heart.     

Salutary effect of nifedipine in pacing-induced angina: relation to afterload reduction

To determine the mechanisms responsible for beneficial effects of nifedipine in pacing-induced angina pectoris, 20 patients undergoing diagnostic cardiac catheterization were studied. Following left ventriculography and coronary arteriography, right atrial pacing was performed before and 30 min after administration of 20 mg of nifedipine sublingually. Heart rate was increased by 10-beat-per-minute (bpm) increments every 90 sec until angina occurred. Electrocardiogram, central aortic pressure, and pulmonary arterial occlusive pressure were monitored continuously. Mean paced heart rate at the onset of angina was increased from 107 +/- 12.6 bpm to 140.6 +/- 19.9 (P less than .001) after nifedipine. Systolic arterial pressure at the time of angina declined from 143 +/- 20 mm Hg to 112 +/- 23 mm Hg (P less than .001). Consequently, the double product heart rate X systolic blood pressure was not changed significantly at the onset of chest pain (149 +/- 28 mm Hg X 10(-2) vs. 142 +/- 28 mm Hg X 10(-2) ). Pulmonary arterial occlusive pressure also did not change significantly (10.4 +/- 4.4 vs. 10.5 +/- 5.9 mm Hg). Thus, nifedipine decreased myocardial oxygen demand at a given heart rate by reducing left ventricular afterload, but did not increase the rate pressure product threshold for ischemic pain. These results indicate that peripheral arterial vasodilator effects of nifedipine, with a resultant decrease in myocardial oxygen requirements, account for its antianginal effect in this setting in patients with fixed obstructive coronary artery disease.     

Short-term control of supraventricular tachycardia with verapamil infusion and calcium pretreatment

Nineteen consecutive patients with atrial fibrillation/flutter or other types of supraventricular tachycardia were given intravenous (IV) calcium salts (1 g) followed by verapamil infusion at a rate of 1 mg/min. Successful treatment was defined as control of ventricular response to less than or equal to 100 beats per minute (bpm) or conversion to sinus mechanism in patients with atrial arrhythmias: 11 patients had atrial fibrillation; three had atrial flutter; four had reentrant supraventricular tachycardias (SVT); and one had paroxysmal SVT. Therapy was successful in all patients. The mean dose of verapamil required to achieve desired outcome was 20 mg. Heart rate showed no significant change as a result of calcium pretreatment (160 bpm v 151 bpm). However, heart rate was significantly decreased, to 95 bpm, after treatment with verapamil. Blood pressure showed no change from baseline with either calcium or verapamil therapy. Verapamil infusion following IV calcium successfully treats atrial fibrillation/flutter or SVTs without depressing systemic blood pressure.     

美托洛尔静脉注射治疗快速心房颤动疗效评价

目的:观察美托洛尔(商品名:倍他乐克)注射液治疗快速心房颤动(房颤)的疗效及安全性。方法:42例快速房颤患者随机分为美托洛尔组与西地兰组,美托洛尔组21例予美托洛尔注射液5～15mg静脉注射,西地兰组21例予西地兰注射液0.4～0.8mg静脉注射,分别观察治疗前及治疗后40min、60min及120min患者心率及血压的变化。结果:1.2组患者分别有12例和8例在120min内心室率降至<100次/min,2组比较差异无显著性(57.14%vs38.09%,P>0.05)。2.美托洛尔组患者心室率降至<100次/min所需的时间为(18.33±12.31)min,西地兰组心室率降至<100次/min所需的时间为(65.00±35.05)min,2组比较差异有显著性(P<0.01)。3.美托洛尔静注起效平均时间(14.00±9.95)min,西地兰静注起效平均时间为(62.50±41.66)min,二者比较差异有显著性(P<0.01)。4.美托洛尔组总有效率85.71%(18/21),西地兰组总有效率47.62%(10/21),2组比较差异有显著性(P<0.01)。5.美托洛尔组治疗主要不良反应为低血压,无心力衰竭及严重心律失常。结论:美托洛尔静脉注射治疗快速房颤安全有效,为急诊科治疗快速房颤的可靠方法。     

26例心房颤动患者心律转复前后心肺运动试验分析

目的探讨心房颤动对心脏功能的影响及心房颤动患者转复心律前后摄氧量等运动参数的改变。方法采用美国MedGraphics公司心肺运动仪和活动平板,在Bruce改良方案的基础上,对26例心房颤动患者分别进行心律转复前后心肺运动试验。结果26例心房颤动患者心律转复后,静息心率(HRrest)平均由109次min减慢到83次min(P<0001),最大运动时心率(HRmax)平均由182次min减慢到141次min(P<0001);最大每搏摄氧量(VO2maxHR)平均由788mL提高到109mL(P<0001);运动总时间(TET)平均由81min增加到88min(P<0001);最大运动速度(Speed)平均由30mph增加到33mph(P<001);斜度(Elevation)由1315%提高到1385%(P<001),试验过程中无并发症发生。结论心房颤动患者转复窦性心律后,心率明显减慢,最大每搏摄氧量增加,运动时间延长,运动耐力提高,心功能得到改善。     

Time-series analysis of heart rate variability during submaximal exercise. Evidence for reduced cardiac vagal tone in animals susceptible to ventricular fibrillation

Periodic fluctuations in the R-R interval have been used as noninvasive measures of cardiac autonomic tone. For example, a reduced heart rate variability has been shown to correlate with an increased mortality in patients recovering from myocardial infarction. The effects that physiologic perturbations such as exercise have on this heart rate variability have not been investigated. Therefore, heart rate variability was measured throughout a submaximal exercise test in 36 mongrel dogs with healed anterior myocardial infarctions. The amplitude of the respiratory component (0.24-1.04 Hz) was determined by time-series analysis techniques and was used as an index of cardiac vagal tone. On a subsequent day, a 2-minute coronary occlusion was initiated during the last minute of exercise. Twenty-two animals developed ventricular fibrillation (susceptible), whereas 14 animals did not (resistant). Exercise elicited a significantly greater increase in heart rate (resistant, 205.4 +/- 7.1; susceptible, 227.0 +/- 5.4 beats/min) in susceptible animals, which was accompanied by a greater reduction in the cardiac vagal tone index (resistant, 2.7 +/- 0.3; susceptible, 1.1 +/- 0.2 ln msec2) as compared with resistant animals. Conversely, atropine sulfate (50 micrograms/kg) given during exercise elicited a greater heart rate increase in the resistant dogs (heart rate change: resistant, 54.2 +/- 7.0; susceptible, 18.7 +/- 4.4 beats/min). Taken together, these data suggest that exercise elicited a greater reduction in cardiac vagal tone in animals known to be susceptible to ventricular fibrillation.     

Long-term calcium antagonist treatment of human hypertension with mibefradil or amlodipine increases sympathetic nerve activity

OBJECTIVES: Calcium antagonists are vasodilating drugs, which may cause reflex activation of the sympathetic nervous system with potentially untoward effects. We studied the effects of long-term treatment with amlodipine, a long-acting dihydropyridine-type calcium antagonist, and mibefradil, a phenylalkylamine-type calcium antagonist, on sympathetic nerve activity. METHODS: Fourteen patients with primary hypertension participated in a double-blind, cross-over study comparing the effects of 6 weeks of treatment with mibefradil 100 mg daily and amlodipine 10 mg daily. Heart rate, direct arterial blood pressure and cardiac output by echocardiography were registered. Global sympathetic activity was estimated using a [3H]noradrenaline isotope dilution method with arterial and venous sampling; cardiac sympathetic activity was assessed indirectly by heart rate variability and tissue velocity echocardiography. RESULTS: Both drugs lowered mean arterial pressure; the decrease was more pronounced with mibefradil (from 118 +/- 3 to 99 +/- 2 mmHg, compared to 118 +/- 3 to 104 +/- 2 mmHg for amlodipine, P < 0.01 between drugs). Mibefradil decreased heart rate (66 +/- 2 to 57 +/- 2 bpm), whereas amlodipine caused a slight increase (66 +/- 2 to 70 +/- 2 bpm; P < 0.001 between drugs) and tended to increase cardiac output. Noradrenaline spillover increased similarly with the two drugs, from 3.44 +/- 0.27 to 5.20 +/- 0.48 nmol/min per m2(P < 0.01) during mibefradil and to 5.72 +/- 0.49 nmol/min per m2 (P < 0.001) during amlodipine. There were minor effects on cardiac sympatho-vagal balance, but systolic and diastolic myocardial velocities were increased similarly by both drugs. CONCLUSIONS: Mibefradil and amlodipine treatment increase global sympathetic nerve activity similarly during long-term treatment, despite opposite effects on heart rate. Increases in myocardial velocities suggest concomitant cardiac sympathetic activation.     

Relationship between sympathetic neural activity, coronary dynamics, and vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion

The relationship between neural sympathetic discharge and vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion was studied in 26 chloralose-anesthetized dogs. Preganglionic cardiac sympathetic impulse activity and ventricular fibrillation thresholds were separately determined before and during a 10-minute period of left anterior descending coronary artery occlusion and during release-reperfusion. Within 2 minutes of occlusion the ventricular fibrillation threshold was significantly decreased (from 25 +/- 1.3 to 16 +/- 2.3 mA, p less than 0.05) corresponding with the period of maximal activation of cardiac sympathetic preganglionic fibers (from 4.4 +/- 0.2 to 6.3 +/- 0.5 impulses/sec). Coronary sinus blood flow and oxygen tension decreased significantly. All these changes persisted for 5 to 6 minutes, thereafter returning to control levels despite continued obstruction of the coronary artery. A transient but significant reduction in ventricular fibrillation threshold also occurred with release of the occlusion but was unaccompanied by increases in sympathetic neural discharge. Bilateral stellectomy completely prevented the ventricular fibrillation threshold changes observed during coronary artery occlusion. However, there was no change in coronary sinus oxygen tension or blood flow. During reperfusion, stellectomy increased rather than decreased vulnerability to ventricular fibrillation. Stellectomy augmented the reactive hyperemic response to release-reperfusion. These findings indicate that enhanced cardiac sympathetic neural activity contributes to ventricular vulnerability associated with coronary artery obstruction. An opposite action results during release-reperfusion. Cardiac sympathetic neural discharge, by reducing the magnitude of reactive hyperemic response through influence on coronary vascular tone, exerts an antifibrillatory effect.     

The effects of atrial fibrillation on regional blood flow in the awake dog

To determine the acute effects of atrial fibrillation on regional blood flow, measurements were made in awake dogs with this arrhythmia induced and sustained by rapid atrial stimulation. Atrial fibrillation reduced cardiac output (from 3.7 +/- 0.3 to 3.0 +/- 0.2 L/min, P less than 0.05), but mean aortic and left atrial pressures were not changed. Although average ventricular myocardial blood flow remained the same, dogs with an average basal myocardial blood flow less than 106 mL/min/100g showed an immediate increase (from 85 +/- 5 to 120 +/- 9 mL/min/100g, P less than 0.05), whereas those with a higher basal value showed a decrease (from 144 +/- 14 to 110 +/- 18 mL/min/100g, P less than 0.05). Moreover, change in myocardial blood flow with atrial pacing, at a rate equal to the average ventricular rate of atrial fibrillation, was directionally similar to that found during atrial fibrillation. However, left atrial myocardial blood flow increased significantly both during atrial fibrillation and pacing. Sustained atrial fibrillation resulted in a fall in splanchnic and renal cortical flow. Brain blood flow also decreased during atrial fibrillation. While the fall in cerebral blood flow was immediately evident, in the cerebellum and brain stem, this decrease was not statistically significant until the 15 min measurement. Also, presence of a ligated common carotid artery did not influence cerebral regional blood flow either under basal conditions or with atrial fibrillation. Thus, in awake dogs the fall in cardiac output that occurs with atrial fibrillation may be accompanied by diverse effects on regional circulations.     

Metabolic and hemodynamic consequences of sodium bicarbonate administration in patients with heart disease

PURPOSE: The use of sodium bicarbonate (NaHCO3) in cardiopulmonary arrest has been questioned, but the effects of NaHCO3 in patients with heart disease are not known. We therefore prospectively evaluated the effects of NaHCO3 in patients with congestive heart failure. PATIENTS AND METHODS: Ten patients received NaHCO3 and control infusions of equimolar sodium chloride (NaCl). Measurements were made of blood gases, 2,3-diphosphoglyceric acid (2,3-DPG), glucose, lactate, cardiac hemodynamics, and oxygen consumption. RESULTS: The arterial oxygen tension (pO2) fell an average of 10 mm Hg after NaHCO3 administration in patients with congestive heart failure, whereas it rose with NaCl (p less than 0.005). Myocardial oxygen consumption decreased by 17% (p less than 0.002) without an accompanying change in oxygen demand. Systemic oxygen consumption fell by 21%. Red blood cell 2,3-DPG levels were elevated at baseline, but did not change with NaHCO3 administration. The oxygen pressure at 50% hemoglobin saturation (P50) was correspondingly elevated at baseline in these patients and decreased significantly with NaHCO3 (Bohr effect) (p less than 0.003). The arterial and mixed venous carbon dioxide tensions increased with NaHCO3 but decreased with NaCl administration (p less than 0.05). Blood glucose concentrations fell by 1.7 mmol/L with NaHCO3 (p less than 0.003) and blood lactate concentrations increased uniformly (p less than 0.001). Three patients developed net myocardial lactate generation during NaHCO3 administration; two of these three developed symptoms of angina. Coronary blood flow did not change with NaHCO3 but increased with NaCl (p less than 0.04). Two patients developed transient pump failure. CONCLUSION: These data demonstrate that NaHCO3 impairs arterial oxygenation and reduces systemic and myocardial oxygen consumption. The decrease in oxygen utilization is associated with anaerobic metabolism, enhanced glycolysis, and elevation of the blood lactate level, and may lead to transient myocardial ischemia in some patients. Thus, the use of NaHCO3 in such patients warrants re-evaluation.     

Effects of atrial fibrillation on myocardial blood flow in the ischemic heart of the dog

Atrial fibrillation has a variable effect on myocardial blood flow in the intact heart. To assess its action on myocardial blood flow in the ischemic heart, measurements were made in nine dogs after ligation of the left anterior descending coronary artery before and during atrial fibrillation and with atrial pacing at the average ventricular response during atrial fibrillation. During atrial fibrillation, cardiac output decreased (from 2.4 +/- 0.2 to 1.5 +/- 0.2 liters/min, p less than 0.001) and mean aortic pressure decreased (from 90 +/- 9 to 72 +/- 7 mm Hg, p less than 0.001). Mean myocardial blood flow decreased from 63 +/- 9 to 51 +/- 9 ml/min per 100 g. Although myocardial blood flow decreased in ischemic myocardium (from 28 +/- 5 to 16 +/- 2 ml/min per 100 g, p less than 0.001), in nonischemic myocardium the changes were more variable (from 71 +/- 8 to 61 +/- 8 ml/min per 100 g, p = NS). During atrial pacing, mean and nonischemic regional myocardial blood flow were comparable with that in atrial fibrillation, whereas in the ischemic region, myocardial blood flow (20.3 +/- 3 versus 14.6 +/- 2.3 ml/min per 100 g, p less than 0.01) and left ventricular inner/outer layer ratio (0.43 +/- 0.07 versus 0.32 +/- 0.06, p less than 0.05) were lower. ST segment elevation increased with both atrial fibrillation (by 89 +/- 31%, p less than 0.05) and atrial pacing (by 51 +/- 28%). Thus, atrial fibrillation has an unfavorable influence on myocardial blood flow in the ischemic heart and worsens myocardial ischemia. This effect is at least in part due to the rapid ventricular rate.     

Ventricular fibrillation occurring after atrioventricular node ablation despite minimal difference between pre- and post-ablation heart rates

We report the case of an 82-year-old man presenting with ventricular fibrillation (VF) occurring acutely after atrioventricular node (AVN) ablation. This patient had severe valvular cardiomyopathy, chronic atrial fibrillation (AF), and underwent prior to the AVN ablation a biventricular implantable cardiac defibrillator positioning. The VF was successfully cardioverted with one external electrical shock. What makes this presentation original is that the pre-ablation spontaneous heart rate in AF was slow (84 bpm), and that VF occurred after ablation despite a minimal heart rate drop of only 14 bpm. VF is the most feared complication of AVN ablation, but it had previously only been described in case of acute heart rate drop after ablation of at least 30 bpm (and more frequently > 50 bpm). This case report highlights the fact that VF may occur after AVN ablation regardless of the heart rate drop, rendering temporary fast ventricular pacing mandatory whatever the pre-ablation heart rate.     

Does atrial overdrive pacing prevent paroxysmal atrial fibrillation in paced patients?

The role of atrial overdrive pacing for the suppression of paroxysmal atrial fibrillation remains unclear. To investigate this we have performed a randomised study evaluating the role of an increased atrial base rate in suppressing this arrhythmia in patients implanted with a permanent pacemaker (Chorum ELA) for sick sinus syndrome with previous documented paroxysmal atrial fibrillation. Twenty-seven patients (mean age, 69; 15 female) were randomised to two 3-month single-blinded crossover periods of DDDR pacing. The pacemaker was set with a base rate of 60 bpm (normal) during one period and at 10 bpm (overdrive) above the average heart rate during the other, mean (S.D.) 75+/-7 beats/min (range, 70-96). The fallback algorithm of the pacemaker was activated to record the number and duration of paroxysmal atrial fibrillation episodes. During the overdrive period there was a significant increase in the total duration of atrial pacing (normal 60+/-26% vs. overdrive 72+/-28%, P<0.001). However there was no significant difference in the number of paroxysmal atrial fibrillation episodes (normal 43+/-109 vs. overdrive 43+/-106, P=ns), or their total duration (normal 42+/-108 h vs. overdrive 99+/-254 h, P=ns). In conclusion, atrial overdrive pacing, achieved by increasing the atrial base rate, has no incremental benefit in the suppression of paroxysmal atrial fibrillation when compared to rate responsive pacing with a base rate of 60 bpm.     

静脉及口服胺碘酮重叠应用治疗器质性心脏病心房颤动伴快速心室率的临床疗效

观察重叠应用静脉及口服胺碘酮治疗器质性心脏病阵发心房颤动 (简称房颤 )伴快速心室率的临床疗效及安全性。 36例器质性心脏病合并房颤的患者 ,男 2 2例、女 14例 ,年龄 6 5 .3± 11.5 (49～ 80 )岁。房颤发作时心室率142 .5± 2 5 .2 (12 0～ 176 )次 /分 ,先给予静脉负荷量胺碘酮 (15 0～ 30 0mg)后 ,继之以 6 0 0 μg/min静脉点滴维持 48h ,同时口服胺碘酮 6 0 0mg/d治疗。结果 :36例患者用药后 30min、1,2 ,2 4,48h心室率分别为 12 4.1± 11.5 ,113.3±8.6 ,10 5 .1± 8.2 ,92 .7± 8.5 ,88.6± 9.4次 /分 ,较用药前明显下降 (P <0 .0 1)。 30例 (83 .3% )患者转复为窦性心律 ,于 2h ,2～ 2 4h ,2 4～ 48h ,2～ 7d转复率分别为 11.1%、2 7.8%、2 2 .2 %和 2 2 .2 %。未转复组患者左房径大于转复组(P <0 .0 5 ) ,而射血分数明显低于转复组 (P <0 .0 5 ) ,这可能是 6例患者未转复的原因。 2例患者用药后出现长RR间期 ,1例出现窦性心动过缓 ,1例出现双手震颤 ,经减药或停药后恢复。结论 :静脉及口服胺碘酮重叠应用治疗器质性心脏病房颤是有效和安全的。