Functional significance of transient collaterals during coronary artery spasm

Coronary collateral vessels appear transiently during vasospasm. To examine the functional role of such collaterals in acute myocardial ischemia, regional coronary flow was determined in patients who showed isolated total spasm in the proximal left anterior descending coronary artery associated with (n = 7, group I) and without (n = 9, group II) collaterals, which were donated by the nonspastic right coronary artery during ergonovine provocative test. Aortic pressure and heart rate were not significantly different in the 2 groups before and during spasm. During vasospasm, the levels of pulmonary artery end-diastolic pressure were significantly higher in group II (19 +/- 2 mm Hg, mean +/- standard error) than in group I (15 +/- 1 mm Hg, p less than 0.05). Under these conditions, great cardiac vein flow (GCVF) measured by thermodilution was markedly reduced in group II (from 60 +/- 4 ml/min to 37 +/- 4 ml/min, p less than 0.01), whereas GCVF was slightly reduced in group I (from 56 +/- 4 ml/min to 51 +/- 4 ml/min), indicating that residual GCVF was greater in patients with than in those without collaterals (p less than 0.05). The calculated coronary collateral resistance index during vasospasm was significantly lower in group I (2.06 +/- 0.18 mm Hg min/ml) than in group II (2.91 +/- 0.30 mm Hg min/ml, p less than 0.05). Total left anterior descending coronary artery spasm with collaterals was less frequently associated with ST elevation in the precordial electrocardiogram recorded during spasm.(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of head-up tilt test in the evaluation and management of unexplained syncope or pre-syncope

This study included 87 consecutive patients with unexplained syncope or pre-syncope who had undergone the head-up tilt (HUT) test with concomitant isoproterenol infusion. A positive response was defined as development of syncope or pre-syncope in association with substantial hypotension (decline of systolic blood pressure > or = 20 mmHg). Coronary artery spasm was suggested from the clinical symptoms and electrocardiographic findings in 1 patient (1/87= 1.1%). Intolerance to isoproterenol infusion was noted in 8 cases (8/87 = 9%). Of the 78 patients who completed the study, 73 showed positive responses (73/78 = 94%). (baseline systolic blood pressure = 125 +/- 23 mmHg endpoint systolic blood pressure = 76 +/- 11 mmHg, p < 0.05; baseline heart rate = 73 +/- 14 beats per minute vs endpoint HR = 80 +/- 24 beats per minute, p < 0.05). In 73 patients who showed positive responses, the systolic blood pressure (SBP) and heart rate (HR) returned to a safe level at 2 minutes when the patients were returned to a supine position (post-study 2 minutes SBP = 124 +/- 18 mmHg vs baseline SBP 125 +/- 23 mmHg, p = NS; post-study 2 minutes HR = 82 +/- 18 beats per minute vs baseline HR = 73 +/- 14 beats per minute, p < 0.05). All 73 patients with a positive HUT test received Atenolol therapy (50 mg daily). Only 35 of these 73 patients took Atenolol regularly and had a repeat HUT test. After atenolol therapy, persistent positive responses were observed in 19 cases (19/35 = 54%) and negative responses were noted in 16 cases (16/35 = 46%). The mean dosage of isoproterenol needed to provoke a positive HUT test in 19 patients who had received Atenolol therapy and had a positive repeat HUT test was 2.3 +/- 1.2 microg/min at baseline and 3.5 +/- 0.9 microg/min for post-Atenolol therapy (p < 0.001). Sixteen patients with a negative repeat HUT test were treated continuously with Atenolol and followed for a mean period of 13 +/- 11 months (range, 1-34 months). All 16 patients were free of syncope or pre-syncope during the period of follow up. In conclusion, the HUT test is mostly well tolerated and safe, even though the test has a low rate of adverse effects. Atenolol is effective for the prevention of provoked or spontaneous recurrent syncope or pre-syncope.     

Coronary arterial spasm in angina at rest associated with transient ST-segment changes

In order to clarify the role of coronary arterial spasm in the pathogenesis of angina at rest, coronary arteriography was performed during spontaneous chest pain or following intravenous administration of ergonovine maleate in 40 patients with angina at rest. Coronary vasospasm was demonstrated in 23 patients with ST-segment elevation during chest pain (group I), in 7 with ST-segment depression (group II), and in 4 with both ST-segment depression and elevation (group III). Complete spastic occlusion of the proximal or of the midportion of the left anterior descending artery was always associated with ST-segment elevation in anterior leads. In contrast, transient ST-segment depression in anterior leads was associated with diffuse narrowing of the left anterior descending artery with slow progression of the contrast medium, or complete occlusion of a small branch or of the distal segment of the left anterior descending artery. ST-Segment elevation in inferior leads was associated with complete spastic occlusion or with significant spastic narrowing of the right coronary artery or of the circumflex artery. We conclude that coronary spasm can be demonstrated in a selected cohort of patients with angina at rest associated with transient ST-segment changes. In some cases the site and the severity of the spasm may produce varying degrees of ischemia, thus determining the direction of the ST-segment shift.     

Clinical characteristics of patients with exercise-induced ST-segment elevation without prior myocardial infarction.

BACKGROUND: Exercise-induced ST-segment elevation is a relatively uncommon problem and occurs more frequently in patients who have had a myocardial infarction. Data is limited on the characteristics of Taiwanese patients without prior myocardial infarction who develop exercise-induced ST-segment elevation. METHODS AND RESULTS: Exercise-induced ST-segment elevation developed in 9 of 6,147 consecutive patients without myocardial infarction who underwent treadmill exercise testing at out institution over a 4-year period. The clinical and angiographic characteristics of these patients were studied. Angiographically normal coronary arteries with coronary vasospasm were found in 5 patients, hemodynamically significant coronary stenosis was found in 3 patients, and coexisting spasm in angiographically normal coronary arteries combined with hemodynamically significant coronary stenosis in the different vessel was found in 1 patient. During a median follow-up of 71 months, 2 patients with coronary vasospasm developed recurrent angina after self-discontinuation of calcium antagonists and 2 patients (1 with coronary vasospasm and 1 with hemodynamically significant coronary stenosis) died of cardiac causes before arrival at the emergency department. CONCLUSION: Coronary vasospasm was a more common underlying pathology of exercise-induced ST-segment elevation in this Taiwanese cohort. Coronary angiography +/- intracoronary ergonovine provocation testing is necessary in these patients to identify the underlying pathology and appropriate treatment.     

Magnesium deficiency in patients with recent myocardial infarction and provoked coronary artery spasm.

This study sought to clarify the relationship between magnesium (Mg) deficiency and coronary artery spasm provoked by pharmacologic agents in patients with a recent acute myocardial infarction (AMI). Twenty-three consecutive patients suffering from AMI were investigated with a Mg retention test (Mg: 0.1 mmol/kg for 4 h) in both the acute phase (within I week (3+/-2 days) of onset) and the subacute phase (3-4 weeks (24+/-6 days) of the onset). Early coronary arteriography was performed in all patients. Coronary stenosis in the infarct-related artery was less than 90% in all patients in the subacute phase. The spasm provocation test was performed in the subacute phase and coronary spasm was defined as transient subtotal or total occlusion in association with angina or electrocardiographic ST-segment deviation. Coronary artery spasm was provoked in only 13 of the 23 patients. Compared with the control subjects (12 patients without coronary artery disease or coronary spasm), the 24-h Mg retention was significantly higher in patients with AMI (acute phase: 78+/-27%, subacute phase: 66+/-32%, vs control: 48+/-12%, p<0.05). In the subacute phase, the 24-h Mg retention decreased in patients without coronary spasm (43+/-26%), but a high level of Mg retention was still observed in patients with coronary spasm (84+/-25%). There was no difference in the serum concentrations of Mg, calcium and phosphorus between the 2 groups on both phases. In conclusion, both Mg deficiency and provoked coronary artery spasm were noted in more than half of the Japanese patients with a recent AMI, suggesting a close association between Mg deficiency and AMI.     

The incidence and morphology of ischaemic ventricular tachycardia

Ventricular arrhythmias are a frequent cause of sudden death in patients with coronary artery disease. The incidence and relationship of ventricular tachycardia to periods of myocardial ischaemia in these patients has not been fully investigated. Ambulatory ST-segment monitoring was performed in 100 consecutive patients with chest pain, of whom 74 had significant coronary artery disease. Recordings were analysed for ST-segment changes and episodes of ventricular tachycardia (greater than 3 beats, rate greater than 100 beats min-1). None of the 26 patients with normal coronary arteries, one of the 22 patients (4.5%) with single vessel disease, one of the 22 patients (4.5%) with double vessel disease and four of the 30 patients (13%) with triple vessel disease, had episodes of non-sustained ventricular tachycardia. Four of these six patients had episodes of reversible ST-segment change but ventricular tachycardia was related to these episodes in only two patients. These two patients had multiple episodes of tachycardia which occurred after the onset of ST-segment change and terminated before the ST-segment returned to baseline; they occurred in clusters with a mean of 12 episodes in each cluster. ST-segment change did not follow episodes of ventricular tachycardia in any patient. The number of ventricular complexes in each episode varied between three and 24 beats and were uniform in three of the six patients. The mean heart rate before the onset of tachycardia was 79 +/- 8 beats per minute and the rate of tachycardia had a mean of 170 +/- 34 beats a minute. Less than 10% of the episodes had a prematurity index of less than 1.(ABSTRACT TRUNCATED AT 250 WORDS)     

Importance of coronary artery spasm in alcohol-related unexplained syncope.

To examine the role of coronary artery spasm in patients with syncope after alcohol ingestion, we performed an intracoronary ergonovine provocation test in 7 male patients (39 to 73 years old, mean 54 years) with alcohol-related syncope which remained unexplained despite noninvasive cardiovascular and neurological examinations. No patients had structural heart disease or significant coronary artery stenosis. Ergonovine was continuously infused into each coronary artery at a rate of 10 micrograms/min for up to 5 min. Coronary artery spasm with ST-segment elevation was induced in 4 of 7 patients. Chest pain before syncope or history of chest pain were not present in 3 of 4 patients with a positive ergonovine test. Multivessel coronary artery spasm was induced in 3 patients. One patient presented with triple vessel coronary artery spasm progressing to near syncope as a result of profound hypotension and ventricular tachycardia during provocation. Coronary artery spasm was promptly relieved by intracoronary isosorbide dinitrate infusion. All patients with a positive ergonovine test were treated with calcium antagonist and did not experience syncope during follow-up. These results suggest that coronary artery spasm is one of the important causes of syncope after alcohol ingestion.     

Comparative effects of oral molsidomine and nifedipine on methylergometrine-induced coronary artery spasm

Twelve consecutive patients (10 men and 2 women, mean +/- standard deviation age 49 +/- 9 years) with chest pain, angiographically normal coronary arteries and coronary artery spasm documented by methylergometrine testing received a single oral dose of molsidomine (4 mg) or nifedipine (10 mg) in a randomized, double-blind, crossover fashion at a 24-hour interval. Coronary artery spasm was documented during coronary angiography in 6 patients (left anterior descending artery, 3; right coronary artery, 2; left circumflex, 1). In the remaining 6 patients, coronary artery spasm was documented by a positive methylergometrine test performed at the bedside, which provoked ST-segment elevation in the inferior (n = 3), anterior (n = 1) or lateral (n = 2) leads. Ninety minutes after administration of the study medication, methylergometrine testing was performed at the bedside, using incremental doses of up to 0.4 mg of methylergometrine. After molsidomine, 10 patients (83%) had a negative and 2 had a positive test; after nifedipine, 9 patients (75%) had a negative and 3 a positive test. Only 1 patient had a methylergometrine test that remained positive after either molsidomine or nifedipine. Therefore, molsidomine appears as effective as nifedipine in suppressing methylergometrine-induced coronary artery spasm in patients with variant angina. In addition, patients not responding to 1 of the study medications may respond to the other.     

Clinical application of the alkalosis induction test for coronary artery spasm

Alkalosis was used for stress testing for coronary artery spasm in 70 patients (average age: 56 years) with resting angina. A rapid intravenous infusion of an alkaline buffer (THAM) immediately followed by 5 minutes' maximal ventilation increased the arterial pH to 7.67 +/- 0.5. Anginal pain and ECG changes were observed in 24 Patients, with ST elevation in 10 cases and ST depression in 14 cases. The ischaemic changes occurred during hyperventilation in 16 cases and in the 3 minutes following the test in 8 cases. The heart rate increased from 66 +/- II to 71 +/- 14 bpm (p less than 0,01) but systolic blood pressure fell from 139 +/- 12 to 130 +/- 12 mm Hg during hyperventilation; there was no significant change in the rate-pressure product (1130 +/- 1750 to 8990 +/- 2690). In all cases, the angina and ischaemic changes regressed after intravenous Trinitrin. Coronary angiography was performed in 56 patients: in the 24 patients with positive responses (Group I) and in 30 of the 46 patients with negative responses (Group II). Significant coronary artery narrowing (greater than 70%) was observed in 21 patients of Group I: in the 3 patients without coronary lesions an intravenous injection of 0.4 mg methylergometrine provoked coronary spasm. In Group II, significant narrowing was demonstrated in 18 patients: in the 12 other patients, coronary spasm could not be induced by methylergometrine. Therefore, in the absence of organic coronary lesions, an excellent correlation has been shown between the alkalosis and methylergometrine tests. This stress test was repeated in 16 of the 24 patients in Group I one hour after administration of 20 mg of Nifedepine: the test was negative in all cases. We conclude that the alkalosis test could be useful in the coronary care unit as a stress test for coronary spasm to determine the antianginal treatment of choice and to evaluate its efficacity.     

Effects of intracoronary injection of ergonovine on angiographic normal coronary arteries: study of 108 consecutive patients

To assess the local and systemic intracoronary (IC) ergonovine maleate (EM), single or repeated 25 micrograms bolus injections were administered to 108 consecutive patients with chest pain and normal coronary arteriograms. Coronary artery spasm (CAS) was induced in 17 (15.7%) patients. None of these patients developed ST-segment depression, and ST-segment elevation appeared in only 6 (35.3%). In 59 of the 91 patients without CAS, both the IC and the intravenous (IV) EM arteriographic and hemodynamic effects were compared. The mean diameter of the vessels was reduced by 15% (p less than 0.001) after two single 25 micrograms ICEM injections. Only insignificant changes were induced in the heart rate (baseline 80 +/- 15; after ICEM 79 +/- 15 beats/min; p = NS) and systolic aortic pressure (baseline 147 +/- 27; after ICEM 149 +/- 28 mmHG; p = NS). Following 350 micrograms of cumulative IVEM, the mean coronary diameter decreased by 20% (p less than 0.01 vs. ICEM dose) and the heart rate diminished slightly (76 +/- 12 beats/min, p less than 0.01). However, the systolic aortic pressures did increase by 16% (171 +/- 28 mmHg; p less than 0.001). No major complications were observed. Thus, to induce CAS the IC delivery route appears to be safe, allows for more accurate titration, and adverse systemic effects, such as hypertension, are avoided.     

Lack of evidence for alpha-adrenergic receptor-mediated mechanisms in the genesis of ischemia in syndrome X

Patients with syndrome X (typical angina pectoris, positive exercise tests [greater than or equal to 1 mm of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) have a reduced coronary flow reserve due to inappropriate dilatation of small resistive vessels. To assess whether alpha-adrenergic mechanisms play a role in the genesis of ST-ischemic changes in syndrome X, 12 patients with this syndrome (2 men and 10 women, mean age 50 +/- 6 years) underwent exercise testing and 24-hour ambulatory electrocardiographic monitoring. They were done off treatment and after alpha blockade with prazosin and clonidine on 2 separate weeks. Despite treatment, all exercise tests remained positive and patients were stopped because of progressive angina pain. Compared to the off-treatment tests, exercise duration and heart rate-blood pressure product at 1 mm of ST-segment depression did not change significantly after prazosin (617 +/- 203 vs 663 +/- 203 seconds and 23,857 +/- 6,125 vs 22,098 +/- 4,816 beats/min X mm Hg, respectively) and clonidine (684 +/- 148 vs 649 +/- 80 seconds and 25,514 +/- 2,386 vs 24,567 +/- 2,001 beats/min X mm Hg, respectively). Ambulatory monitoring showed similar results regarding number of episodes of ST-segment depression greater than or equal to 0.1 mV during control and after prazosin (39 vs 38) or clonidine (26 vs 23) treatment. None of the 8 patients who also underwent provocative testing with phenylephrine had ischemic electrocardiographic changes; only 2 experienced chest pain during the test.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ability of calcium-entry blockade by felodipine to disclose different pathogenetic mechanisms behind hyperventilation-induced myocardial ischemia in men

To verify that myocardial ischemia occurring during either the overbreathing or recovery phase of the hyperventilation test is based on different pathogenetic mechanisms, 2 consecutive series of patients, selected on the basis of their response to a run-in hyperventilation test, were studied. Group I comprised 15 patients who developed ST-segment depression early during overbreathing, whereas group II consisted of 12 patients showing ST-segment depression late during the recovery phase. A single oral dose of felodipine 10 mg or of placebo was administered on 2 consecutive days according to a randomized, double-blind, crossover design, and the hyperventilation test was repeated, on both days of the study, 3 to 5 hours after drug intake. In group I, ST-segment depression occurred after placebo in all patients during overbreathing, with an increase in rate pressure product (from 112 +/- 31 at baseline to 168 +/- 55 mm Hg x beats/min/100 at the onset of ST-segment depression; p less than 0.01). After felodipine, 13 patients continued to show ST-segment depression during overbreathing, together with an increase in rate pressure product (from 107 +/- 24 at baseline to 158 +/- 46 mm Hg x beats/min/100 at the onset of electrocardiographic changes; p less than 0.01). In group II, all 12 patients showed ST-segment depression during recovery after placebo, with a rate pressure product comparable to baseline conditions (112 +/- 35 at baseline vs 102 +/- 27 mm Hg x beats/min/100 at the onset of ST-segment depression; difference not significant). After felodipine, no patient developed ST-segment depression or chest pain.(ABSTRACT TRUNCATED AT 250 WORDS)     

Paced breathing can prevent vasovagal syncope during head-up tilt testing

BACKGROUND: Clinical experience suggests that, through the control of heart rate, paced breathing may prevent syncope. OBJECTIVE: To assess the effect of metronome-paced breathing (0.2 Hz) on the outcome of head-up tilt test (HUT) in patients with vasovagal syncope. PATIENTS AND METHODS: Ten patients (two men), mean +/- SD age 18.4 +/- 5.1 years, with a positive HUT with spontaneous breathing and no evidence of cardiovascular or neurological disease, were exposed to a second HUT under metronome-paced breathing (0.2 Hz). Continuous electrocardiographic recordings were obtained during the two tests, and heart rate variability was analyzed off-line. RESULTS: During HUT with metronome-paced breathing, only one of the 10 patients developed bradycardia, hypotension and syncope (P<0.01, Wilcoxon). Compared with HUT with spontaneous breathing, HUT with paced breathing induced a larger increase in the heart rate in the first minute of tilt (4 +/- 6 beats/min versus 16 +/- 12 beats/min, P<0.05). CONCLUSIONS: The results show that paced breathing can prevent vasovagal syncope induced by HUT. This finding suggests that respiratory training could be useful to prevent vasovagal syncope.     

The differential response in atrial natriuretic peptide release during exercise in patients with and without ischemic heart disease

The elevation of cardiac filling pressure induces the release of atrial natriuretic peptide into the circulation. Ischemia during exercise in patients with coronary artery disease may manifest itself with elevation of cardiac filling pressure before the onset of electrocardiographic changes or chest pain. Thus, patients with ischemic heart disease might have an elevated circulating atrial natriuretic peptide after exercise. The present study investigated the effect of exercise on circulating atrial natriuretic peptide in patients with and without ischemic heart diseases. Group 1 was composed of five patients who had ischemic heart disease by clinical history, previous myocardial infarction, angina or angiographically proven coronary artery disease and positive electrocardiogram during exercise. Group 2 was composed of five patients without ischemic heart disease and negative electrocardiogram response. Heart rate, blood pressure, and atrial natriuretic peptide were measured during routine treadmill exercise testing using the Bruce protocol. Our results indicate that the rate of rise of heart rate (12.3 +/- 1.8 vs. 8.5 +/- 0.7 beats/min/min), blood pressure (7.1 +/- 1 vs. 4.2 +/- 0.8 mm Hg/minute), and atrial natriuretic peptide (4.1 +/- 1 vs. 1.4 +/- 0.3 pg/ml/min) was significantly elevated in patients with ischemic heart disease compared to the group 2 patients. These findings suggest that the disproportionate elevation of atrial natriuretic peptide after exercise in ischemia may be caused by elevation of cardiac filling pressure, which may provide a noninvasive method for the diagnosis of ischemic heart disease.     

Prevalence of coronary artery spasm during dobutamine stress echocardiography

The aim of this study was to assess the prevalence of coronary artery spasm during dobutamine stress echocardiography (DSE). Over a 9-year period (from November 2001 to October 2010) we reviewed all patients (n = 2,224) referred for DSE. Criteria for selection included patients > 18 years old who underwent DSE. We systematically analyzed all electrocardiograms obtained during DSE to detect ST-segment elevation during the examination. All patients with ST-segment elevation underwent coronary angiography. DSE was performed in 2,179 patients. ST-segment elevation was observed in 21 patients, all of whom underwent emergency coronary angiography. In 13 of these 21 patients (62%) significant coronary stenosis was observed: 6 patients with critical coronary stenosis and 7 patients with chronic coronary occlusion. The remaining 8 patients (38% of patients presenting with ST-segment elevation during DSE, 7 men, mean age 67 ± 11 years) had no significant coronary stenosis. Prevalence of coronary artery spasm during DSE was 0.4%. In conclusion, physicians should be aware that, although rare, coronary artery spasm may occur during DSE.     

Diffuse left ventricular hypokinesis mimicking dilated cardiomyopathy with multi-vessel coronary vasospasm

We investigated 7 patients with multi-vessel coronary vasospasm (> or = 75%) and diffuse left ventricular hypokinesis by coronary angiography and echocardiography. Four patients were male and 3 were female and mean +/- SD age was 63.0 +/- 11.2 years. Chief complaints were dyspnea in 3 patients, and chest pain, appetite loss, palpitation and general fatigue in one each. New York Heart Association functional classification was I in one patient, II in 5 and III in one. Mean heart rate was 73.9 +/- 11.6 beats/min. Initial echocardiography showed left ventricular end-diastolic diameter (LVDd) 54.4 +/- 5.5 mm, left ventricular end-systolic diameter (LVDs) 43.7 +/- 4.8 mm and percentage fractional shortening (%FS) 19.7 +/- 2.6%. The left ventricle was not remarkably enlarged despite poor contraction. Coronary vasospasm was induced after acetylcholine injection into the right coronary artery in 6 patients, left anterior descending artery in 7 and circumflex artery in 5. Four patients developed three-vessel coronary vasospasm. Three patients underwent endomyocardial biopsy which showed non-specific mild fibrosis. They were treated with nitrates and/or Ca-antagonists to prevent coronary vasospasm. Follow-up echocardiography was performed in 6 patients after 8.5 +/- 6.6 months. Echocardiography revealed marked improvement in left ventricular contraction (LVDd 49.7 +/- 4.6 mm, LVDs 35.8 +/- 4.4 mm, p < 0.05; %FS 27.9 +/- 4.5%, p < 0.05). These data suggested that left ventricular dilation was not prominent despite the poor contractility in patients with multi-vessel coronary vasospasm and diffuse left ventricular hypokinesis. The left ventricular dysfunction might be hibernating myocardium produced by multiple episodes of coronary vasospasm. Anti-vasospastic agents were effective in these patients.     

Analysis of heart rate variability during the head-up tilt test in patients with vasovagal syncope

Changes of the autonomous nervous tonus are considered the most important factor in the pathogenesis of vasovagal syncope. In order to investigate changes of the autonomous tonus the authors examined in patients with vasovagal syncope the variability during the head-up tilt test (HUT). In 35 patients with assumed vasovagal syncope the authors used a passive HUT (45 mins., 60 degrees) and subsequently nitroglycerin-stimulated HUT (0.4 mg s.l, 15 mins.). The heart rate variability was evaluated before the onset of the test in a horizontal position, immediately after tilting the patient (0 min.), during the 5th, 10th, 15th minute of the passive test, during the 5th minute of the nitroglycerin test, during the appearance of symptoms and after termination of the test in a horizontal position. They compared the results between a group of 20 patients with positive HUT (13 men, 36 years) and in 15 patients with a negative HUT (7 men, 32 years). The parameters of heart rate variability were during the development of the syncope (mean 6.4 mins. after administration of NTG) as compared with corresponding values in patients with negative HUT (during the 5th minute after administration of NTG) as follows: RR interval 759.6 +/- 248.1 ms vs. 552.1 +/- 88.7 ms (p = 0.01), SDNN 44.8 +/- 49.6 vs. 29.9 +/- 18.3 (p = 0.001), RMSSD 31.8 +/- 34.9 vs. 15.2 +/- 10.2 (p = 0.03), LF 4.44 +/- 0.66 lnms2 vs. 4.38 +/- 0.53 lnms2 (p = 0.82), HF 4.44 +/- 0.57 lnms2 vs. 4.39 +/- 0.45 lnms2 (p = 0.82), LF/HF 0.99 +/- 0.03 vs. 0.99 +/- 0.02 (p = 0.90). On development of the first presyncopal manifestations the statistical parameters of heart rate variability in patients with positive HUT were significantly higher as compared with patients with negative HUT, which suggests an increase of the parasympathetic autonomous tonus during the development of the vasovagal syncope.     

Long-term variability of angina pectoris and electrocardiographic signs of ischemia in syndrome X

The long-term course of angina and the electrocardiographic signs of ischemia were assessed in 13 patients (10 women and 3 men, mean age 49 +/- 6 years) with typical angina pectoris, positive exercise tests, no evidence of coronary spasm and angiographically normal coronary arteries (syndrome X). Clinical and electrocardiographic parameters as well as results of exercise testing and 24-hour electrocardiographic monitoring were assessed at presentation and after a mean follow-up of 6.3 years (range 3 to 9). Mean number of anginal episodes and nitroglycerin consumption per week were similar at presentation and at the last follow-up. Furthermore, no significant difference was noted in heart rate-systolic blood pressure product at 0.1 mV of ST-segment depression (20,363 +/- 5,747 vs 21,649 +/- 5,687 beats/min x mm Hg), at angina (19,223 +/- 5,680 vs 20,126 +/- 6,023 beats/min x mm Hg) and at peak exercise (22,057 +/- 5,669 vs 22,868 +/- 6,122 beats/min x mm Hg). Time to 0.1 mV of ST-segment depression, to angina and to peak exercise was also similar (595 +/- 163 vs 631 +/- 184 s, 524 +/- 156 vs 571 +/- 168 s and 671 +/- 168 vs 718 +/- 186 s, respectively). The number of episodes of ST-segment depression greater than or equal to 0.1 mV during electrocardiographic monitoring was similar at presentation and follow-up (31 vs 25) as was the proportion of painful episodes (39 vs 36%). None of the patients developed major coronary events or cardiomyopathy during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

运动诱发ST段抬高的临床意义

对５例运动诱发暂时性ＳＴ段抬高的原因及其与血管病变的关系进行分析，提出劳力型心绞痛患者运动诱发ＳＴ段抬高的临床意义不同于变异型心绞痛患者，对前者在近期内施行经皮冠状动脉腔内成形术（ＰＴＣＡ）是安全和有效的。运动诱发ＳＴ段抬高恢复正常后，相邻导联的ＳＴ段压低仍持续存在，提示其缺血相关血管有严重阻塞性病变。     

Coronary vasospasm as a potential cause of myocardial infarction and paroxysmal atrial fibrillation in a relatively young woman

Vasospasm-related myocardial infarction in young women with normal coronary arteries has infrequently been reported and vasospasm-related paroxysmal atrial fibrillation (PAF) has rarely been described. We present a 33-year-old woman with old inferior myocardial infarction and postinfarction angina at rest; the angina was accompanied by PAF and electrocardiographic ST-segment elevation in the inferior leads. Coronary angiography revealed normal coronary arteries and intracoronary acetylcholine provoked an intense and diffuse spasm of the right and left coronary artery. The spasm of the right coronary artery was associated with PAF and ST-segment elevation in the inferior leads. Frequently documented PAF, accompanied by chest discomfort and ST-segment elevation in the inferior leads, was more effectively removed with isosorbide dinitrate than with disopyramide. These data suggest that coronary vasospasm is a likely cause of myocardial infarction and even PAF, although the precise mechanism leading to PAF remains unknown.