Carlo Duilio

Relation Between Diastolic Perfusion Time and Coronary Artery Stenosis During Stress-Induced Myocardial Ischemia

BACKGROUND Experimental studies have demonstrated that during stress-induced myocardial ischemia, coronary obstruction and diastolic perfusion time are factors that limit subendocardial perfusion and correlate to degree of myocardial dysfunction. The relation between these two factors has not yet been investigated in humans. The aim of the present study was to assess the relation between diastolic perfusion time and degree of coronary stenosis during different types of stress tests. METHODS AND RESULTS Nine patients with isolated and proximal stenosis of the left anterior descending coronary artery were selected. Patients underwent three different randomized stress tests (upright, supine bicycle stress test, and transesophageal atrial pacing). Diastolic perfusion time, heart rate (RR interval), and systolic and diastolic pressures were measured during the test and at the ischemic threshold (0.1-mV ST-segment depression). Angiographic measurements of coronary stenosis were evaluated by quantitative coronary angiography. At the ischemic threshold, significant differences among tests were found in heart rate (P < .05), systolic pressure (P < .001), and diastolic pressure (P < .05). In each stress test, diastolic perfusion time at the ischemic threshold was closely correlated with minimal stenosis diameter (r = .97; P < .001) and percent diameter stenosis (r = .92; P < .001) with no difference among the tests. In contrast, heart rate, rate-pressure product, and time to ischemic threshold were not significantly correlated with percent diameter stenosis and minimal stenosis diameter. No significant correlation was observed at the ischemic threshold between diastolic perfusion time and corresponding values of heart rate, despite the close correlation at rest (r = .95; P < .001). CONCLUSIONS Despite differences in associated hemodynamic responses to various stress tests, a close relation exists between stenosis severity and diastolic perfusion time at the onset of stress-induced myocardial ischemia. Therefore, diastolic perfusion time at the ischemic threshold may be an indirect estimate of the hemodynamic significance of coronary stenosis.

Diastolic perfusion time at ischemic threshold in patients with stress-induced ischemia.

BACKGROUND To evaluate the relevance of diastolic perfusion time on the mechanisms underlying stress-induced ischemia, 16 patients with coronary artery disease and seven patients with syndrome X underwent five randomized stress tests (upright and supine exercise with and without therapy, transesophageal atrial pacing). METHODS AND RESULTS Exercise duration Time to 0.1 mV ST segment depression, heart rate, rate-pressure product, and diastolic perfusion time were evaluated for each patient during stress tests. In both groups, variability coefficients of the above-mentioned parameters were not different at rest. At ischemic threshold (0.1 mV ST segment depression) in patients with coronary artery disease, the variability coefficient of exercise duration (40.1 +/- 22.2) was significantly higher (p less than 0.0001) than those of heart rate (12.8 +/- 2.9), rate-pressure product (14.8 +/- 3.3), and diastolic perfusion time (0.39 +/- 0.1). The variability coefficient of diastolic perfusion time was also significantly (p less than 0.0001) lower than those of heart rate and rate-pressure product. Similarly, the variability coefficient of diastolic perfusion time (0.44 +/- 0.1) in syndrome X patients was significantly lower (p less than 0.0001) than those of exercise duration (28.2 +/- 9.4), heart rate (12 +/- 1.4), and rate-pressure product (14.6 +/- 1.3). CONCLUSIONS Fixed diastolic perfusion time at ischemic threshold, despite different kinds of stress tests and variability of heart rate and rate-pressure product, indicates the relevant role of diastolic perfusion time in determining myocardial ischemia.

Effects of beta blockade on the relation between heart rate and ventricular diastolic perfusion time during exercise in systemic hypertension

Abstract It is well known that cardiovascular response to exercise involves sympathetic stimulation of the heart and peripheral vessels and that β blockade interferes with adrenergic response during exercise. When a decrease in heart rate is prevented by atrial pacing, regional myocardial function and blood flow in ischemic areas tend to be more depressed after β blockade, suggesting that β blockade could unmask an α 2 adrenergic vasoconstriction, worsening regional blood flow and function. 1 An alternative hypothesis might be that β blockade modifies the relation between diastolic time and heart rate. In fact, there is also some evidence that β blockade impairs the postexercise diastolic time in patients with coronary artery disease. 2 However, this effect is not clearly explained, since ischemia alone could interfere with diastole duration. 3,4 Moreover, the effect of β blockade on diastolic time during exercise is still unknown. This study investigates the effects of β blockade on diastolic time during exercise in hypertensive patients without stress-induced myocardial ischemia.

Electromechanical Events during Spontaneous Angina

The electromechanical events occurring during acute myocardial ischemia were assessed in 10 patients who developed spontaneous angina during cardiac catheterization. Aortic pressure and electrocardiogram were recorded, and heart rate and systolic and diastolic time intervals were measured under control conditions, at the onset of angina and during the relief of chest pain. In 5 patients spontaneous angina was accompanied by an increase in heart rate and systemic arterial pressure and by ST segment changes in anterior or anterolateral precordial leads. Diastolic time, expressed as percent of cardiac cycle, shortened from 48.8 +/- 3.6% at rest to 33.6 +/- 4.8% (p less than 0.01) at the onset of angina, as a consequence of a significant increase in both electromechanical systole and heart rate, and returned to control values within 10 min after sublingual nitroglycerin. In the remaining 5 patients, spontaneous angina was accompanied by a decrease in heart rate and systemic arterial pressure and by ST segment changes in the inferior or inferolateral leads. The diastolic time increased significantly (p less than 0.05) from 39.4 +/- 6.1% at rest to 47.8 +/- 9% at the onset of angina, as a consequence of a significant decrease in heart rate and a slight decrease in electromechanical systole. Since coronary perfusion takes place mainly during diastole, our results suggest that the reflex increase in adrenergic tone may worsen myocardial ischemia by affecting diastolic perfusion time. In contrast, the increase in vagal tone may contribute to spontaneous relief of angina by prolonging diastolic perfusion time.

Haemodynamic effects of dual-chamber pacing versus ventricular pacing during a walk test in patients with depressed or normal left ventricular function.

PurposeDual-chamber rate-modulated pacing provides haemodynamic benefits compared with ventricular pacing at rest, but it is unclear whether this also holds true during physical exercise in patients with heart failure. This study assessed the haemodynamic response to a walk test during dual-chamber pacing and ventricular pacing in patients with depressed or normal left ventricular (LV) function.MethodsTwelve patients with an LV ejection fraction <50% and 11 patients with an LV ejection fraction ≥50% underwent two randomised 6-min walk tests under dual-chamber rate-modulated pacing and ventricular pacing at a fixed rate of 70 beats/min. All patients had a dual-chamber pacemaker implanted for complete heart block. LV function was monitored by a radionuclide ambulatory system.ResultsIn patients with depressed LV function, the change from dual-chamber pacing to ventricular pacing induced a decrease in end-systolic volume at the peak of the walk test (P<0.05), with no difference in end-diastolic volume. As a consequence, higher increases in LV ejection fraction (P<0.0001) and stroke volume (P<0.01) were observed during ventricular pacing. No difference in cardiac output was found between the two pacing modes. In patients with normal LV function, the change from dual-chamber pacing to ventricular pacing induced a significant decrease in cardiac output (P<0.005 at rest and P<0.05 at the peak of the walk test).ConclusionCompared with dual-chamber rate-modulated pacing, ventricular pacing improves cardiac function and does not affect cardiac output during physical activity in patients with depressed LV function, whereas it impairs cardiac output in those with normal function.

Site of myocardial ischemia as a determinant of postexercise blood pressure and heart rate response in coronary artery disease

Forty patients with coronary artery disease and 15 normal subjects (group C) were studied to assess the influence of the site of stress-induced myocardial ischemia on cardiovascular response after exercise. Patients were divided in 2 groups according to myocardial thallium-201 scintigraphy: those with an anteroseptal reversible perfusion defect (group A; n = 24), and those with an inferoposterior reversible perfusion defect (group I; n = 16). All patients underwent serial bicycle exercise stress tests. The first 2 stress tests were interrupted when 0.1 mV of ST-segment depression was achieved (2,000 to 2,500 kg-m); a third test was stopped before the onset of ischemia (1,500 kg-m). Normal subjects performed stress tests at comparable work loads. At ischemic threshold, there was no difference in ejection fraction between groups A (65.5%) and I (67.3%). Mean values and recovery ratios of heart rate and systolic blood pressure were significantly higher in group A than in C and I during the recovery period of the 2,000 to 2,500 kg-m stress test. In contrast, no significant difference was observed among the groups in the 1,500 kg-m stress test, and between groups I and C in any stress test. The data show that in patients with the same degree of stress-induced impairment of ventricular function, the anterior site of ischemia leads to persistently higher values of heart rate and blood pressure after exercise, which are likely due to an enhanced adrenergic discharge.

Different Automatic Mode Switching in DDDR Pacemakers

Mode-switching algorithms are designed to alleviate symptoms related to tracking of atrial arrhythmias, that may result in inappropriately rapid or irregular ventricular pacing[1–19]. The ideal mode-switching algorithm should discriminate sinus tachycardia, a rhythm that should be tracked, from pathological atrial arrhythmias, rhythms that generally should not be tracked. In order to minimize symptoms related to the occurrence of atrial arrhythmias, the mode-switching algorithm should change quickly from a tracking to a non-tracking mode at the onset of the pathological atrial rhythm and remains in this mode until the arrhythmia terminates. Once sinus rhythm has been restored, the pacemaker should revert quickly to the normal atrial tracking mode. There are several potential causes of symptoms that relate to mode switching. First, an irregular paced ventricular intervals at the onset of an atrial arrhythmia before conversion to a non-tracking mode. Second, failure of the device to convert to a non-tracking mode because of intermittent undersensing of the atrial electrocardiogram may result in continued irregular or rapid ventricular pacing [20]. Third, inappropriate reversion to a tracking mode despite persistence of an atrial arrhythmia may also be caused by intermittent undersensing of the atrial electrocardiogram. Fourth, an overly sensitive mode-switching algorithm may result in loss of atrio-ventricular (AV) synchrony in sinus rhythm [2,11,17,19]. Finally, intrinsic AV conduction of an atrial arrhythmia may produce symptoms that are unrelated to the pacemaker [21]. Although all manufacturers of dual chamber pacemakers offer devices that provide mechanisms for managing the occurrence of atrial arrhythmias, the mode-switching algorithms that are available differ significantly in their sensitivity, specificity, and speed of mode conversion at the onset and termination of atrial arrhythmias. There are potential compromises between sensitivity and specificity with these algorithms, the balance of which may determine the frequency of arrhythmia-related symptoms. Atrial-based pacing is associated with a risk of developing atrial fibrillation lower than ventricular-based pacing for patients with sinus node dysfunction [22-25].

Diastolic Perfusion Time and Exercise Posture in Coronary Artery Disease Patients: Correlation with ST Segment Changes

The relationship between either heart rate or diastolic time and ST segment depression has been evaluated during supine and upright exercise in 16 coronary artery disease patients. Diastolic perfusion time and ST segment depression were related by a linear regression, which was independent of exercise posture. The entity of ST segment depression was greater during supine than in upright exercise for the same heart rate. The assessment of the relationship between heart rate and diastolic perfusion time during two exercises showed that at the same heart rate, diastolic perfusion time was shorter in supine posture. In conclusion, the greater entity of ST segment depression induced by supine rather than upright exercise might be explained by the effect of supine posture on diastolic perfusion time.

Alinidine in Chronic Stable Angina: The Effect on Diastolic Perfusion Time

The present study has been performed to assess the effects of alinidine on diastolic duration during exercise in chronic coronary artery disease. Twelve male patients with stable effort angina and without previous myocardial infarction were studied. They received alinidine or placebo in a double-blind randomized crossover trial for 3 days after a wash-out period of 4 days. Alinidine was administered at a dosage of 30 mg 3 times a day. At the end of each treatment the patients underwent upright bicycle exercise. Left ventricular time intervals were obtained by means of carotid thermistor plethysmography. Diastolic duration was calculated by subtracting the electromechanical systole from the R-R interval and expressed as a percentage of the cardiac cycle (%D). Alinidine increased both total exercise duration from 246.7 +/- 120.7 to 346.6 +/- 114.1 s (p less than 0.05) and time to 0.1-mV ST segment depression from 98.3 +/- 53 to 187.2 +/- 105 s (p less than 0.05). Similarly the drug induced a reduction of the rate-pressure product and of the extent of ischemic ST segment depression during exercise. %D was increased by alinidine both at rest and during exercise. A direct linear regression between R-R and %D was found after both alinidine and placebo treatments either at rest or during exercise. Nevertheless, no difference was observed between both slopes and intercepts. Therefore, since the relationship between R-R interval and %D was unaffected by alinidine, it was possible to hypothesize that the changes in diastolic duration were due only to the bradycardic action of the drug.

Ear arterial pulse computation reliability of diastolic perfusion time during stress test

Diastolic perfusion time is a critical determinant of myocardial oxygen supply when coronary artery flow is limited by a significant stenosis of the coronary vessel. Diastolic time adjustment of the ST segment depression occurring during effort enhances stress test prediction of the coronary impairment severity. Effective diastolic adjustment of ST segment requires a stable and simple to perform measurement of the diastolic perfusion time during stress test execution. The authors investigated the reproducibility of the diastolic measurements obtained using the arterial pulse of the lobulus auriculae compared to the classical phonocardiographic data. The results obtained indicate that ear arterial pulse measurement of the diastolic time is reliable avoiding the difficulties rising from using the phonocardiographic method.