A rare combination of coronary anomalies.

Coronary anomalies are found in less than 1% of diagnostic coronary angiograms. The clinical relevance of these anomalies varies from insignificant to potentially lethal. The major role of coronary angiography in interventional cardiology and coronary surgery underscores the importance of having knowledge of the variations in coronary anatomy and their clinical relevance. We report a rare case of a patient with a combination of coronary anomalies: coronary fistulae, a double circumflex coronary artery and anomalous origin of a circumflex artery from the proximal right coronary artery. (Neth Heart J 2008;16:387-9.).

Coronary angiographic findings do not predict clinical outcome in patients with unstable angina.

OBJECTIVES: The presence of thrombus formation and type of coronary artery lesion were determined in patients with unstable angina and correlated with the angiographic findings and clinical outcome. BACKGROUND: Some previous studies have suggested that thrombus formation and lesions are predictive of the angiographic and clinical findings. This was evaluated in a retrospective analysis of 159 patients participating in the placebo-controlled Unstable Angina Study Using Eminase (UNASEM) trial on the effect of thrombolysis in unstable angina. METHODS: Patients without a previous myocardial infarction who presented with a typical history of unstable angina in the presence of abnormal findings on the electrocardiogram indicative of ischemia were included in the study. After baseline angiography, study medication (anistreplase or placebo) was given to 126 to 159 patients. Thirty-three patients did not receive medication because of significant main stem disease or normal coronary arteries or for other reasons. Angiography was repeated after 12 to 28 h. RESULTS: Quantitative angiography showed a significant decrease in diameter stenosis in the anistreplase-treated group compared with the placebo-treated group (decrease 11% vs. 3%, p = 0.008). No differences in clinical outcome were found when thrombolytic treatment was compared with placebo (p = 0.98). Neither the presence nor absence of thrombus formation (p = 0.98) nor the type of lesion (p = 0.96) was related to the changes in diameter stenosis or to clinical outcome (p = 0.90 and p = 0.77, respectively). The power of these analyses to detect a 20% difference varied between 56% and 74%. CONCLUSIONS: In this selected group of patients with unstable angina, type of coronary artery lesion and the presence or absence of thrombus formation does not predict clinical outcome.

Prognostic value of Q waves, R/S ratio, loss of R wave voltage, ST-T segment abnormalities, electrical axis, low voltage and notching: correlation of electrocardiogram and left ventriculogram.

Data on the correlation of left ventricular segmental wall motion and electrocardiographic findings are, except for Q waves and ST segment elevation, still controversial. Therefore, in addition to Q waves and ST segment elevation, eight features of the electrocardiogram were studied in 265 patients, 61 with normal coronary arteries and 204 with coronary artery disease. Patients with a QRS duration of 0.12 second or greater were excluded. Left ventricular wall motion was assessed in the 30 degrees right anterior oblique and the 60 degrees left anterior oblique projections and analyzed by the Stanford method and a modification of that method, respectively. Asynergy of a particular segment correlated well with the presence of Q waves in the corresponding electrocardiographic lead or leads, but was also found in other segments. There was a significant (p less than 0.001) correlation between the number of leads with Q waves and the degree of extension of asynergy. The R/S ratio in lead V1 and Q waves in lead V6 appeared to be the most informative about the posterior wall. Loss of R wave voltage had a lower predictive value for segmental asynergy than did Q waves in the same lead. Among patients with electrocardiographic findings of an infarct, asynergy was found in 83 to 94%. Patients having Q waves in combination with ST segment elevation manifested more severe asynergy than did patients whose Q waves were not associated with ST elevation. New data are presented for lateral and posterior infarction. Patients having left-axis deviation, low voltage and QRS notching had severe asynergy.(ABSTRACT TRUNCATED AT 250 WORDS)

Abciximab in the treatment of acute myocardial infarction eligible for primary percutaneous transluminal coronary angioplasty. Results of the Glycoprotein Receptor Antagonist Patency Evaluation (GRAPE) pilot study.

OBJECTIVES: We sought to study the effect of early infusion of abciximab on coronary patency before primary angioplasty in patients with acute myocardial infarction. BACKGROUND: Glycoprotein IIb/IIIa antagonists have proved to be effective in reducing ischemic events associated with coronary angioplasty. The present study explores whether abciximab alone, without administration of thrombolytic therapy, may induce reperfusion in patients with acute myocardial infarction. METHODS: In the Glycoprotein Receptor Antagonist Patency Evaluation pilot study 60 patients with less than 6 h signs and symptoms of acute myocardial infarction eligible for primary angioplasty received in the emergency room a bolus of abciximab 250 microg/kg followed by a 12-h infusion of 10 microg/min. All patients were also treated with an oral dose of 160 mg aspirin and 5,000 IU of heparin intravenously. As soon as possible a diagnostic angiography was performed to evaluate the patency of the infarct-related artery. RESULTS: The median time between onset of symptoms and the administration of the abciximab bolus was 150 min (range 45 to 345), and the median time between abciximab bolus and first contrast injection in the infarct-related artery was 45 min (range 10 to 150). In 24 patients (40%, 95% confidence interval 28% to 52%) Thrombolysis in Myocardial Infarction (TIMI) flow grade 2 or 3 was observed at a median time of 45 min (range 10 to 150) after abciximab bolus; TIMI flow grade 3 was observed in 11 patients (18%, 95% confidence interval 9% to 28%). There was no difference in percentage of TIMI flow grade 2 or 3 between patients who received abciximab within 2.5 h after onset of symptoms or thereafter. CONCLUSIONS: Abciximab therapy given in the emergency room in patients awaiting primary angioplasty is associated with full reperfusion (TIMI flow grade 3) in about 20% and with TIMI flow grade 2 or 3 in about 40% of the patients at a median time of 45 min. These figures are higher than those in primary angioplasty trials without such pretreatment. Randomized controlled trials of very early infusion of abciximab, either prehospital or in-hospital, in patients eligible for angioplasty are warranted.

Does angiography six months after coronary intervention influence management and outcome? Benestent II Investigators.

OBJECTIVES: This study was performed to assess whether angiography six months after coronary balloon angioplasty or stent implantation has an influence on clinical management and one-year outcome. BACKGROUND: The Benestent II study randomized 827 patients to balloon angioplasty or stent implantation. A subrandomization was undertaken allocating patients to six-month clinical follow-up (CF) or clinical and angiographic follow-up (AF). METHODS: Seven hundred and six patients (349 CF and 357 AF) had no intercurrent angiography, so that restenosis and disease progression elsewhere remained unknown until the time of six-month follow-up. These two groups, which were well matched at enrolment, were compared with respect to symptoms, medication and major cardiac events defined as death, myocardial infarction and need for revascularization at six and 12 months. RESULTS: At six-month follow-up, 53 (15%) of the CF and 76 (21%) of the AF patients had stable angina (p = 0.041), while 5 (1%) and 4 (1%) had symptoms of unstable angina. At 12-month follow-up, 44 (13%) patients in both groups had stable angina, and only 1 patient in the CF group had unstable angina. Seventy-seven patients (27 CF and 50 AF; p < 0.01) had major cardiac events between 6 and 12 months. Of the 349 patients in the CF group, 21 underwent repeat percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery between 6 and 12 months, compared with 44 of the 357 patients in the AF group (relative risk 2.05 [1.24 to 3.37], p = 0.003). CONCLUSIONS: Patients who had AF six months after balloon angioplasty or stent implantation experienced more repeat revascularization procedures than those who had CF. They also had significantly more angina at six-month follow-up but this may be due to bias.

Effects of thrombolytic therapy in unstable angina: clinical and angiographic results.

The incidence of intracoronary thrombus and the effects of thrombolytic therapy were studied in 41 patients with unstable angina. All patients underwent coronary angiography 2 to 69 h (mean 19) after their last attack of chest pain. Immediately after angiography, 21 patients received intracoronary streptokinase (250,000 IU in 45 min) and were retrospectively analyzed. Twenty patients received intravenous recombinant tissue-type plasminogen activator (rt-PA) (100 mg in 3 h) and were involved in a prospective study. Eleven of the 21 patients from the streptokinase group and 11 of the 20 patients from the rt-PA group showed a decrease in the severity of the coronary stenosis on repeat angiography 1 day later. A decrease in coronary obstruction was primarily observed in 10 of 13 patients with a complete stenosis and in 6 of 9 patients with a subtotal stenosis and markedly diminished coronary flow. Improvement in coronary anatomy was not determined by the clinical characteristics of the patients. Twenty-eight of the 41 patients had angiographic evidence of intracoronary thrombus formation before and 16 had such evidence after thrombolytic treatment. Nine patients developed a small increase in serum cardiac enzymes before or during treatment. Ischemic symptoms and the incidence of surgical or angioplastic intervention were not different in patients with or without a reduction in coronary artery stenosis after fibrinolytic therapy. These observations suggest a high incidence of coronary thrombosis in patients with unstable angina. The data do not permit assessment of the clinical therapeutic efficacy of thrombolytic therapy. Better risk stratification and placebo-controlled prospective studies are required to obtain information on the risk/benefit ratio of such therapy in unstable angina.

Lipid peroxidation-associated oxidative stress during percutaneous transluminal coronary angioplasty in humans.

Animal studies suggest that myocardial ischemia/reperfusion causes oxidative stress. We, therefore, examined whether routinely performed percutaneous transluminal coronary angioplasty (PTCA) might be a human ischemia/reperfusion model for oxidative stress-induced lipid peroxidation. Fasting antecubital venous blood was sampled from 13 patients on the morning of PTCA, and 2 d after PTCA. Venous and coronary arterial blood were sampled just before and 10 min after the first balloon inflation. Samples were analyzed for plasma and LDL lipid hydroperoxide levels, in vitro oxidation of LDL, and LDL antioxidant levels. Lipid hydroperoxide levels in plasma and LDL remained unchanged throughout the study. During the first 10 min of PTCA, the lag time during oxidation of LDL in vitro did not change, but the maximum rate of oxidation decreased in venous and arterial samples (Wilcoxon signed rank test: p < .002). At the same time, total tocopherol levels in LDL significantly increased by 6.3% (p = .048) in arterial, but not in venous samples. Total carotenoid levels increased by 3.8% (p = .127) in arterial samples and decreased by 2.9% (p = .040) in venous samples. Forty hours after PTCA, LDL oxidation parameters and LDL antioxidant levels were similar to baseline, except for about 17% lower levels of delta-tocopherol (p = .037) and gamma-tocopherol (p = .014). Our results, therefore, do not support that PTCA in humans is associated with oxidative stress-induced lipid peroxidation.

The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex.

To determine the value of the electrocardiogram for differentiating aberrant conduction from ventricular ectopy, findings were retrospectively reviewed from patients with a widened QRS complex during tachycardia in whom the site of origin of tachycardia was determined by His bundle electrography. Seventy episodes of sustained ventricular tachycardia from 62 patients and 70 episodes of aberrant conduction during supraventricular tachycardia from 60 patients were available for study. Findings suggesting a ventricular origin of tachycardia were (1) QRS width over 0.14 sec, (2) left axis deviation, (3) certain configurational characteristics of QRS and (4) atrioventricular (A-V) dissociation. Capture or fusion beats resulting from A-V conduction of dissociated atrial complexes during ventricular tachycardia were seen during only four of 33 episodes of sustained tachycardia.

Medical treatment of ventricular tachycardia: considerations in the selection of patients for surgical treatment.

The decision of when and how to treat ventricular tachycardia is primarily determined by the type and severity of concomitant heart disease. After the ventricular origin of the tachycardia is established, extensive investigation into this problem is mandatory. Long-term medical treatment in patients with ventricular tachycardia in the setting of coronary artery disease is unsatisfactory. Although drug selection with the use of programmed cardiac stimulation seems logical and promising, the long-term value of this method remains to be demonstrated. The extensive myocardial damage present in most patients with coronary artery disease and ventricular tachycardia makes it unlikely that drug therapy will be the ultimate answer. These considerations justify careful evaluation of the long-term efficacy of surgical therapy of symptomatic ventricular tachycardia, especially in patients with arrhythmia in the subacute or chronic phase of myocardial infarction.

Differential diagnosis of tachycardia with narrow QRS complex (shorter than 0.12 second).

One hundred eighty-seven patients with clinically documented supraventricular tachycardia with a narrow QRS complex were admitted for electrophysiologic study. The diagnoses after this study were circus movement tachycardia using an accessory pathway in 50 patients, atrioventricular nodal tachycardia in 50 patients, atrial flutter in 50 patients, atrial tachycardia in 27 patients and an incessant tachycardia retrogradely using a slowly conducting accessory pathway in 10 patients. On retrospective analysis, 5 criteria on the 12-lead electrocardiogram during tachycardia were analyzed for their value in making the diagnosis of site of origin. These criteria were P-wave location, axis of the P wave, atrial rate, alternation of the QRS complex and atrioventricular relation. Fifty-seven patients with a narrow QRS tachycardia were prospectively studied using the 5 criteria. A correct diagnosis was made in 48 of the 57 patients (84%). Thus, in most patients with a narrow QRS tachycardia, information from the 12-lead electrocardiogram is adequate for diagnosis.

Initiation and termination of ventricular tachycardia by supraventricular stimuli. Incidence and electrophysiologic determinants as observed during programmed stimulation of the heart.

In 7 of 43 patients in whom a sustained ventricular tachycardia could be induced during programmed electrical stimulation by a single ventricular premature stimulus, an identical tachycardia could also be initiated by a single atrial premature stimulus. This phenomenon was observed only in those patients in whom the ventricular tachycardia could be induced by a single ventricular extrastimulus having a prematurity index (ratio between the longst ventricular premature stimulus interval resulting in tachycardia and th duration of the basic cycle length of the paced ventricular rhythm) above 54 percent. No single instance of initiation of ventricular tachycardia by atrial premature stimuli was observed in patients with a ventricular prematurity index below 54 percent or requiring more than one consecutive ventricular extrastimulus to have tachycardia initiated. Other features of patients showing initiation of ventricular tachycardia by atrial premature stimuli were a right bundle branch block configuration of the QRS complex during tachycardia in all seven patients and a relatively slow rate during tachycardia. In one patient ventricular tachycardia was terminated by a conducted atrial premature stimulus.

Effect of drugs in the Wolff-Parkinson-White syndrome. Importance of initial length of effective refractory period of the accessory pathway.

The effect of procainamide, quinidine, ajmaline and amiodarone on the effective refractory period of the accessory pathway in the (A-V) anterograde and retrograde directions was studied in relation to the length of this period before drug administration. All patients had the Wolff-Parkinson-White syndrome and were studied with intracavitary recordings and programmed electrical stimulation of the heart using identical basic cycle lengths and test stimulus intervals before and after drug administration. The patients were separated into two groups, those in whom the effective refractory period of the accessory pathway was 270 ms or greater (Group 1) and those in whom it was less than 270 (Group 2). In the anterograde direction the magnitude of increase in the length of the effective refractory period of the accessory pathway after drug administration was related to its initial length. Only modest lengthening of this period could be accomplished in patients with an initially short period. In evaluating the effect of drugs in patients with the Wolff-Parkinson-White syndrome, the role of the initial length of the effective refractory period of the accessory pathway should be considered.

Reciprocal tachycardias using accessory pathways with long conduction times.

Three patients with reentrant tachycardia are described who had an accessory pathway with a very long conduction time that was incorporated in the tachycardia circuit. The accessory pathway was able to conduct in one direction only, in retrograde manner in two patients and in anteriograde manner in the remaining patient. Evidence is presented that reveals that in the first two patients the accessory pathway was septally located, had completely bypassed the normal atrioventricular (A-V) conduction system, had properties of decremental conduction, and had an atrial exit close to the coronary sinus and a ventricular exit relatively far from the atrioventricular A-V ring. In the third patient, who manifested wide QRS complex during tachycardia, the ventricular end of the accessory pathway seemed to be located close to the right ventricular apex. The atrial end of the pathway could not be localized exactly.

Use of ajmaline in patients with the Wolff-Parkinson-White syndrome to disclose short refractory period of the accessory pathway.

Ajmaline given intravenously produced complete anterograde block in the accessory pathway of 32 of 59 patients with the Wolff-Parkinson-White syndrome. An electrophysiologic investigation performed 1 day later revealed that failure of ajmaline to produce complete anterograde block in the accessory pathway corresponded to a short refractory period of this pathway (less than 270 ms). The use of ajmaline intravenously is advanced as a reliable and rapid procedure for identifying those patients with the Wolff-Parkinson-White syndrome who have a short refractory period of the accessory pathway and are possible at risk of circulatory insufficiency or sudden death if atrial fibrillation supervenes.

Initiation of ventricular tachycardia by interpolated ventricular premature depolarizations.

Programmed electrical stimulation of the heart was performed in a 47 year old man with prior myocardial infarction and recurrent sustained ventricular tachycardia that was refractory to standard medical therapy. The tachycardia could be provoked by regular atrial pacing at a rate of 100/min, regular ventricular pacing at the same rate and regular atrial pacing at a rate of 200/min in the presence of 2:1 atrioventricular block. All three techniques resulted in an interval of approximately 600 ms between successive ventricular depolarizations. Single interpolated ventricular premature depolarizations delivered during sinus rhythm were followed by a postextrasystolic conducted sinus beat that initiated ventricular tachycardia. However, when the same interpolated ventricular premature depolarization was followed by a ventricular fusion beat no tachycardia ensued. This study therefore emphasizes the importance of hart rate and pattern of ventricular activation in determining whether ventricular tachycardia can be provoked by programmed electrical stimulation of the heart.

Development of ST-segment elevation and Q- and R- wave changes in acute myocardial infarction and the influence of thrombolytic therapy.

Sequential electrocardiograms for admission to 36 hours in 358 patient s with acute myocardial infarction (AMI) from the Pro-urokinase In Myocardial Infarction trial were assessed. The electrocardiogram was also examined at discharge in 69 of 358 patients. Patients underwent acute angiography, after which angioplasty was performed in most patients with impaired flow. The sum of the ST-segment deviation and Q- and R- wave voltages, and the QRS score were calculated and used for further evaluation. Development of Q waves, lost of R waves, and QRS score were completed within the first 9 hours after onset of AMI and remained stable thereafter. Reperfused patients had earlier stabilization and less severe electrocardiographic (ECG) abnormalities than nonreperfused patients. ST-segment elevation had already stabilized after 5 hours, was unchanged at 36 hours, and had significantly decreased at discharge. No significant ECG and clinical outcome differences were found between the Thrombolysis In Myocardial Infarction trial (TIMI) 2 and TIMI 3 patients. A 23.3% gain in ECG-estimated infarct size was found in the reperfusion group compared with a 12.0% gain in the nonreperfused group (p = 0.08). In summary, as early as 9 hours after onset of AMI, QRS changes were already complete. Thereafter, QRS morphology was stable. Thus, a QRS-based estimation of infarct size can be made as early as 9 hours after AMI. A similar ECG outcome for patients with TIMI 2 and 3 flow was found, which was significantly different from patients with TIMI 0 to 1 flow.

Electrical management of arrhythmias with emphasis on the tachycardias.

Information from stimulation studies in human beings with tachycardia has resulted in the application of cardiac pacing in the treatment of such patients. Short-term pacing is especially useful in patients with atrial flutter. Long-term pacing with use of chronically implanted units can be applied to patients with different types of supraventricular and ventricular tachycardia. In these patients careful electrophysiologic studies are required before the pacing device is implanted. New developments enabling automatic and more individually designed modes of pacing are urgently needed.

Effect of procainamide, propranolol and verapamil on mechanism of tachycardia in patients with chronic recurrent ventricular tachycardia.

The effect of short-term intravenous administration of procainamide (12 patients), propranolol (4 patients) and verapamil (4 patients) was studied in 12 patients with chronic recurrent sustained ventricular tachycardia. In all patients tachycardia could reproducibly be initiated and terminated with programmed electrical stimulation of the heart. Procainamide (1) lengthened the effective refractory period of the right ventricle, (2) affected the tachycardia zone, (3) reduced ventricular rate during tachycardia, and (4) lengthened the interval between the tachycardia-initiating premature ventricular beat and the first QRS complex of tachycardia. No effect on the refractory period of the right ventricle or the mechanism of tachycardia was seen after administration of propranolol or verapamil. Apart from their therapeutic implications these data suggest that it may be possible to use drugs to study mechanisms of ventricular tachycardia in the human heart.

Termination of circus movement tachycardia utilizing an accessory atrioventricular pathway by retrograde concealed penetration of the atrioventricular node through the bundle branch system. A mechanism of tachycardia termination in Wolff-Parkinson-White syndrome.

A 30 year old woman with Wolff-Parkinson-White syndrome underwent electrophysiologic study for investigation of circus movement tachycardia utilizing the accessory pathway for retrograde conduction. The accessory pathway was located on the right side. Episodes of circus movement tachycardia with left and right bundle branch block were induced. Some episodes of circus movement tachycardia with left bundle branch block terminated spontaneously. Two episodes of spontaneous termination at the level of the atrioventricular (A-V) node were preceded by prolongation of the H-V interval causing delay in atrial activation. This delayed atrial cycle was then followed paradoxically by spontaneous termination of the tachycardia in the A-V node. A similar phenomenon could be demonstrated reproducibly with single echo beats induced by coronary sinus extrastimuli. It appears that retrograde concealed penetration of the A-V node through the bundle branch system during anterograde left bundle branch block is the most likely mechanism for this phenomenon.

Observations in patients showing A-V junctional echoes with a shorter P-R than R-P interval.

Single test stimulation of the ventricle revealed initiation of echoes with a supraventricular QRS complex with a shorter P-R than R-P interval in 28 of 300 patients consecutively studied with programmed electrical stimulation of the heart because of documented or suspected tachycardias. In all 28 the initiation of echoes was related to a discontinuity in the retrograde conduction curve. In 10 patients a different atrial activation sequence in the endocavitary leads was present before and after the discontinuity in the retrograde conduction curve. In five of these a sustained tachycardia with a shorter P-R than R-P interval could be initiated, and in all five patients an accessory pathway with a long conduction time as the retrograde arm of the tachycardia circuit could be demonstrated. In these five patients spontaneous initiation of tachycardia was observed during sinus rhythm or after atrial premature beats. Tachycardia accelerated after the administration of atropine. In the remaining 23 patients the initiation of echoes showing a shorter P-R than R-P interval was nonsustained. In these patients spontaneous initiation of such echoes during sinus rhythm or initiation by atrial premature beats was not observed, and echoes with this relation of the P-R and R-P intervals systematically disappeared after administration of atropine. It is postulated that in these patients a slow atrioventricular (A-V) nodal pathway is used in the retrograde direction during echoes showing a shorter P-R than R-P interval. Sustained A-V junctional tachycardia showing this relation between P-R and R-P intervals favors incorporation of an accessory pathway with slow retrograde conduction in the tachycardia circuit.