Internal mammary arteriography without selective cannulation using a new balloon occlusion catheter.

Internal mammary artery (IMA) angiography can be difficult and time-consuming. We evaluated a custom designed balloon-tipped catheter, a Berman catheter (Arrow International, Reading, PA) modified by creating an end-hole to allow passage of a wire through the central lumen, for imaging the IMA without selective cannulation. We compared ease of use, procedure time, and image quality of the new catheter with the standard selective catheter technique. Thirty-six patients with IMA grafts were randomly assigned to imaging with either the study catheter or a standard catheter. Image quality, graded from poor to excellent, time to catheter placement in the subclavian artery (TIME 1), time to initial IMA angiography (TIME 2), and the difference between these two (TIME 3) were recorded. TIME 3 defined the time required to find and seat the catheter at the IMA site. The image quality was good or excellent in all but one patient. This one patient, randomized to the standard catheter technique, had poor image quality with the selective catheter. However, exchange for the study catheter resulted in excellent image quality. There was no difference in TIME 1 (P = 0.57) or TIME 2 (P = 0.55) between the two techniques. There was a significant difference in TIME 3 (P = 0.05) favoring the study catheter. There were no complication using either technique and the total contrast volume used was not significantly different between the two techniques (P = 0.32). We conclude that a new catheter technique for imaging the IMA without selective cannulation is safe, fast, easy to use, and may offer particular advantage in patients whose internal mammary artery is difficult to access.

Signal-averaged ECG prior to and serially after thrombolytic therapy for acute myocardial infarction.

Signal averaging has been performed to evaluate late potentials following infarction and the administration of thrombolytic therapy. Most studies have recorded signal-averaged electrocardiograms (SAECGs) at least 12 hours after the onset of the infarction. In this study, SAECGs were recorded before thrombolytic therapy and serially over 7-10 days following infarction in 21 patients. The high frequency QRS duration was significantly shortened at 1 and 24 hours compared to presentation (96.8 +/- 11.3 ms and 93.4 +/- 8.0 ms vs 103.3 +/- 14.3 ms, respectively, P < 0.05) and there was an increase in the terminal voltage over time, significant at 1 hour and 3 days (57.3 +/- 29.1 microV and 58.6 +/- 44.7 microV vs 44.4 +/- 35.5 microV, respectively, P < 0.01). Five patients met criteria for ventricular late potentials on at least one SAECG. The prevalence of late potentials was higher in patients with Q wave infarctions, or with occluded infarct related arteries. These changes in myocardial activation may be related to ischemia and reperfusion, and may not correlate with the development of a fixed substrate for reentry.

Effects of exercise on signal-averaged electrocardiogram.

Signal averaging can be used to assess changes in myocardial activation under a variety of physiological conditions including stress. This study prospectively evaluated patients who underwent rest and exercise recording of signal-averaged electrocardiograms. The 163 patients were divided into three groups based on thallium results: normal (group I), reperfusion (group II), and fixed defect (group III). Patients in group I showed shortening of the high frequency duration (P = 0.02) and the duration of the low amplitude signal (P = 0.024) after exercise. In these patients the terminal root mean square amplitude (RMSA) also increased significantly (P = 0.005). However, patients who were in either group II or group III showed little change in signal averaging measurements after exercise. The amplitude of the QRS in V5 and the RMSA of the total QRS also increased in all groups following exercise, with a lesser increase in the patients with reperfusion by thallium imaging (group II). There was no change among groups in the incidence of ventricular late potentials with exercise. This suggests that patients with ischemia or infarction may not have the same response to an increase in sympathetic tone with exercise as patients without abnormalities of cardiac perfusion. The clinical implications of these findings may include demonstration that an area of slow conduction exists in these latter two groups of patients.

Adverse effects of calcium binding contrast agents in diagnostic cardiac angiography. A comparison between formulations with and without calcium binding additives.

RATIONALE AND OBJECTIVES: The authors compared complications and hemodynamic and electrophysiologic effects of two formulations of diatrizoate, one with additives that bind calcium and one without, in diagnostic cardiac angiography. METHODS: Two hundred twenty-three consecutive low-risk patients alternately received Hypaque 76 (group 1, little calcium binding effect), and MD 76 (group 2, significant calcium binding). Electrocardiographic and hemodynamic changes related to coronary angiography and left ventriculography were measured, and complications requiring treatment were recorded. RESULTS: There were more complications in patients in group 2 than in group 1 (18 versus 8, P = 0.04). Arterial pressure fell more, the QT interval increased more, and the heart rate fell more in group 2 after coronary angiography. CONCLUSIONS: Formulations of diatrizoate that minimize calcium binding are advocated for cardiac angiography when using high osmolality contrast media. The more detrimental effects that calcium binding has on myocardial function and cardiac conduction may lead to the higher incidence of complications.

Perceived and actual risks of driving in patients with arrhythmia control devices.

BACKGROUND: We surveyed patient attitudes about driving and about driving restrictions for patients with automatic defibrillators and pacemakers, and we assessed risk of arrhythmias occurring during driving. METHODS: One hundred two patients responded to a questionnaire (57 patients with defibrillators and 45 patients with pacemakers) about driving habits and opinions on restriction of patients who have devices and want to drive. In addition, the literature was reviewed for approximate incidences of sudden death and syncopal or nonsyncopal device therapy to estimate risk while driving of having a defibrillator discharge. RESULTS: Thirty-two patients with defibrillators (56%) and 28 patients with pacemakers (62%) currently drove an average of 196 and 161 km/wk, respectively. Most patients felt that driving was a right and 75% felt that restriction imposed a hardship on them. Respondents felt that common sense, limited distances, or physician input should set driving limitations. A minority felt that no restrictions should be placed on these drivers or that they should not drive at all. The risks of sudden death and syncopal and nonsyncopal defibrillator discharge were estimated at 0.0009%, 0.0011%, and 0.0015% per kilometer driven, respectively, based on weekly kilometers and published occurrences of these phenomena. CONCLUSIONS: Patients perceive that driving is their right and that there is a low risk of an arrhythmic event behind the wheel. The estimated risk and published accounts of sudden death support this. However, concurrent medical problems and stresses imposed by driving may increase risk. The physician must make reasonable recommendations to ensure patient and public safety, keeping in mind both state and federal driving regulations and reporting requirements.

Oral amiodarone loading for the rapid treatment of frequent, refractory, sustained ventricular arrhythmias associated with coronary artery disease.

To evaluate the efficacy and safety of oral amiodarone in the treatment of recurrent, sustained, refractory ventricular arrhythmias, rapid high-dose oral loading was used to treat 12 critically ill patients with frequent, sometimes incessant, sustained ventricular arrhythmias refractory to 2 to 6 antiarrhythmic agents. Presenting arrhythmias included sustained monomorphic ventricular tachycardia and ventricular fibrillation associated with cardiac arrests in 6 patients. Patients experienced 2 to 10 episodes (mean 5 +/- 2) of sustained ventricular arrhythmias over a mean period of 6.2 +/- 5.0 days (range 1 to 14) before oral amiodarone was initiated at 1,200 to 1,400 mg/day. This included at least 1 to 4 episodes (mean 2.2 +/- 1.1) within 24 hours before amiodarone. One to 4 antiarrhythmic drugs were administered concurrently during amiodarone loading. Sustained ventricular arrhythmias no longer occurred after a mean of 5.2 days (range 1 to 22) with amiodarone. Arrhythmias were controlled in 4 patients within 24 hours, 5 patients within 48 hours, 7 patients within 4 days and 10 patients within 6 days. Patients experienced a mean of 0.6 +/- 0.8 episodes within 24 hours after amiodarone. Nine patients survived to hospital discharge. No patient had significant adverse effects during high-dose loading. In conclusion, high-dose oral amiodarone loading, when added to previously unsuccessful conventional antiarrhythmic therapy, is safe and often rapidly effective for at least short-term control of frequent, refractory, sustained ventricular arrhythmias.

Atypical presentations and echocardiographic findings in patients with cardiac tamponade occurring early and late after cardiac surgery.

Cardiac tamponade, a potentially lethal complication following cardiac surgery, may present either early or late postoperatively and may be difficult to diagnose due to atypical clinical, hemodynamic, or echocardiographic findings. To determine the frequency and clinical features of postoperative cardiac tamponade, we performed a review of 510 consecutive patients who underwent cardiac surgery. The incidence of postoperative cardiac tamponade was 2.0 percent (10/510 patients) and occurred following valvular, bypass, and aortic surgery. Nine of ten patients had either atypical clinical, hemodynamic, and/or echocardiographic findings. The diagnosis of tamponade was made 1 to 30 days (mean = 8.5 days) postoperatively. Presenting symptoms were often mild and nonspecific. Classic signs including hypotension, pulsus paradoxus greater than 12 mm Hg, and elevated jugular venous pressure were present in 7, 6, and 5 patients, respectively. Right heart hemodynamics revealed elevated and equalized diastolic pressures in three of six patients. Two-dimensional echocardiography revealed selective compression of the left ventricle (LV) (four patients), right ventricle (RV) (one patient), left atrium (LA)/RV (one patient), LA/LV (one patient), LA/LV/RV (one patient), all four chambers (one patient), and no diastolic collapse of any chamber (one patient). There was often an absence of anterior pericardial fluid (six patients) with tethering of a portion of the RV to the chest wall anteriorly (five patients). Coagulation parameters were "supratherapeutic" in only three of eight patients who were receiving systemic anticoagulants at the time of diagnosis. The initial diagnosis was confused with congestive heart failure in one patient, pulmonary embolism in three patients, acute myocardial infarction in two patients, and sepsis in one patient. Eight of ten patients survived; all of these patients underwent surgical removal of fluid and/or hematoma in the operating room. We conclude that postoperative tamponade after cardiac surgery may have varied clinical and hemodynamic presentations, often due to selective chamber compression by loculated fluid or clot. Due to its frequently atypical features and presentation that may simulate other disorders, the diagnosis of tamponade should be considered whenever hemodynamic deterioration or signs of low output failure occur in the postcardiotomy patient.

Antiarrhythmic and pharmacokinetic evaluation of intravenous recainam in patients with frequent ventricular premature complexes and unsustained ventricular tachycardia.

The pharmacokinetics, antiarrhythmic activity and safety of intravenously administered recainam were evaluated in 15 men and 3 women. All patients had frequent (> 30/hour) ventricular premature complexes (VPCs) and unsustained ventricular tachycardia. Recainam was administered at a loading dose of 4.5 mg/kg/hour over 40 minutes, followed by a maintenance infusion of 0.9 mg/kg/hour for 23 hours and 20 minutes. Sixteen patients had satisfactory efficacy data. The mean frequency of total VPCs decreased by 92.6% and the mean frequency of runs decreased by 99.9% during the maintenance infusion. Suppressions of > or = 70% of total VPCs and > or = 90% of runs were maintained over the 23-hour, 20-minute maintenance infusion period in 16 of the 18 patients. During the maintenance infusion, hourly group plasma recainam concentrations ranged from mean +/- SD 2.6 +/- 0.7 to 3.4 +/- 0.9 micrograms/ml. Patients were observed for 24 hours after termination of the infusion. Periodic blood samples were obtained during and after termination of the infusion to determine recainam concentration. Urine specimens were collected over scheduled intervals to determine urinary excretion of recainam. A 2-compartment pharmacokinetic model was used to analyze the data. The following pharmacokinetic parameters were obtained: terminal elimination half-life, 5.0 +/- 0.8 hours; systemic clearance, 0.27 +/- 0.08 liter/hour/kg; and central and steady-state volume of distribution, 0.32 +/- 0.11 and 1.4 +/- 0.4 liter/kg, respectively. Adverse experiences were reported in 4 of the 18 patients, possibly drug-related in 2; none was considered severe or required discontinuation of recainam.(ABSTRACT TRUNCATED AT 250 WORDS)

Combined ambulatory electroencephalographic and electrocardiographic recordings for evaluation of syncope.

Evaluation of patients with syncope often includes a battery of noninvasive tests. In this study, 45 patients (26 with suspected neurologic and 19 with suspected cardiac syncope) were evaluated with simultaneous 24-hour electroencephalographic (EEG) and 2-channel electrocardiographic (ECG) recordings. Isolated cardiac rhythm abnormalities were noted in 21 patients, but none of these was symptomatic and no definitive arrhythmias occurred. Isolated EEG abnormalities were noted in 11 patients, 5 of whom had EEG abnormalities consistent with seizure disorders. Simultaneous EEG and ECG abnormalities were seen in 4 patients. In 2 cases, a previously unsuspected etiology for syncope was found: seizures in 1 patient with heart disease, and sinus pauses in another thought to have a seizure disorder. Thus, combined ambulatory EEG/ECG monitoring may prove useful in the evaluation of some patients with syncope.

Spontaneous changes in ventricular tachycardia cycle length.

Understanding spontaneous fluctuations in ventricular tachycardia cycle length is required to develop algorithms for ventricular tachycardia detection and termination. Variations in cycle length, time to stable cycle length and the range of RR intervals during ventricular tachycardia were analyzed in 74 episodes of sustained monomorphic ventricular tachycardia induced in patients not taking antiarrhythmic medication. Linear regression demonstrated cycle length variability to decrease over time (41 +/- 24 to 17 +/- 19 ms, p less than 0.001). Slower ventricular tachycardia had more cycle length variability than faster ventricular tachycardia (p less than 0.001). Ventricular tachycardia that was initially more variable tended to remain more variable (p less than 0.001). Fifty-four percent of episodes stabilized within the first 15 beats, 75% by 30 beats and 93% by 50 beats. The number of beats to stable cycle length was independent of ventricular tachycardia rate. The average range in cycle length per episode was 127 +/- 72 ms; 12% of ventricular tachycardia episodes varied by less than 50 ms and 45% by less than 150 ms. The maximal range in RR intervals from a single episode of ventricular tachycardia was 290 ms. Therefore, ventricular tachycardia demonstrates a wide range of cycle lengths and has time-dependent changes in variability and stability. These cycle length changes should be considered in the algorithms for ventricular tachycardia detection and termination by automatic antitachycardia devices.

Differentiation of arrhythmias by measurement of intracardiac pressures in man.

Antitachycardia devices currently use sustained high rate, abrupt changes in cycle length, and probability density function to determine the onset of ventricular tachycardia. Hemodynamic changes occur with the onset of tachycardia and may provide a method of discriminating supraventricular from ventricular tachycardia. In this study, patients had atrial and ventricular pressures measured during rapid atrial and ventricular pacing. Right atrial pressure increased significantly with ventricular pacing but not with atrial pacing. Right ventricular pressures did not significantly differ with atrial or ventricular pacing. The change in atrial pressure compared to baseline was greater, with ventricular pacing compared to atrial pacing. Right ventricular pressure increased compared to baseline with atrial or ventricular pacing, but there was no significant difference between pacing modalities. Measurement of right atrial pressure might prove useful in discriminating supraventricular from ventricular tachycardia.

Improvement in early diastolic filling dynamics after aortic valve replacement.

With use of ultrafast computed tomography, 13 patients undergoing aortic valve replacement for aortic stenosis were prospectively followed to evaluate the relation between left ventricular mass and diastolic function. Studies were done before intervention, and then at 4 and 8 months later. Mass decreased from 161 +/- 11 g/m2 (+/- standard error of the mean) at baseline to 106 +/- 5 g/m2, and then to 97 +/- 7 g/m2 at 4 and 8 months, respectively, in 12 patients who demonstrated significant (greater than 20%) mass regression after operation. One patient failed to show significant changes in mass. Diastolic function, as defined by the peak filling rate of early diastole, improved (p less than 0.02) in the group with mass regression, from 2.11 +/- 0.17 s-1 at baseline to 2.12 +/- 0.23 s-1, and then to 2.62 +/- 0.26 s-1 at 4 and 8 months, respectively. Improvement in the time to peak filling rate was also noted. Heart rates were unchanged, whereas end-diastolic volumes decreased and ejection fractions increased slightly. Postoperative increase in peak filling rate correlated with regression of ventricular mass to within normal range (+/- 2 standard deviations) and attainment of New York Heart Association class I status by 8 months (p less than 0.02). Thus, improvement in diastolic function can be seen after aortic valve surgery and is associated with improved functional class. Diastolic function improves later than the regression in wall mass and may imply a delayed remodeling of the ventricle.

Frequency of low-grade residual coronary stenosis after thrombolysis during acute myocardial infarction.

The clinical, angiographic and demographic characteristics of 42 patients with low-grade (less than 50%) residual stenosis at the infarct lesion after thrombolysis for acute myocardial infarction (MI) were assessed. The study group (group I) represented 21% of 198 consecutive patients receiving thrombolytic therapy over a 59-month period. Data on the 156 remaining patients were pooled for comparison (group II). Group I patients were predominantly men (86%) who were cigarette smokers (81%). Group II patients were predominantly men (75%, p greater than 0.10) but were significantly older (52 +/- 12 vs 56 +/- 10 years, p = 0.02). Prior acute MI or angina was unusual in group I. Sixty percent had no significant (greater than 50%) residual coronary artery disease while 25% had residual single artery disease. Average significant (greater than 50% diameter stenosis) residual vessel disease was 0.6 +/- 1.0 for group I and 1.9 +/- 0.9 for group II (p less than 0.001). In group I, average residual infarct lesion diameter stenosis was 36 +/- 7% in the right anterior oblique and 34 +/- 8% in the left anterior oblique views. Thirty-nine group I patients were discharged with medical therapy and 100% follow-up was obtained over a mean interval of 18 +/- 17 months. Fifteen patients experienced chest pain after acute MI accounting for 17 discrete events. Fifty-nine percent of group I had a benign course on follow-up. Eight events were classified as unstable angina, 4 as acute MI and 5 as atypical angina. Documented coronary vasospasm occurred in 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular mass regression after aortic valve replacement measured by ultrafast computed tomography.

Left ventricular mass and function were measured using ultrafast computed tomography, and were correlated with clinical status in 17 patients with aortic stenosis and/or insufficiency undergoing aortic valve replacement or balloon valvuloplasty. Wall mass was 159 +/- 38 gm/m2 initially, decreased 25% to 116 +/- 29 gm/m2 at 4 month (p less than 0.001), and decreased a total of 34% to 105 +/- 33 gm/m2 at 8 months after valve repair. By 8 months not only was the mean wall mass within the normal range, but only three patients retained abnormal hypertrophy. Ejection fraction increased 8% (p = 0.06). Clinical function improved in all patients, with only three patients remaining outside of New York Heart Association functional class 1 at 8 months. Regression of ventricular mass into the normal range correlated with attainment of class 1 functional status (p less than 0.02), despite a lack of increase of ejection fraction. The single patient followed for 8 months after valvuloplasty had minor wall mass regression and minor clinical improvement.

Value of electrophysiologic testing in patients with previous myocardial infarction and nonsustained ventricular tachycardia. Philadelphia Arrhythmia Group.

Previous studies of the value of electrophysiologic studies in patients with nonsustained ventricular tachycardia (VT) have been hampered by the inclusion of a small number of patients with various types of heart disease. This retrospective study was designed to assess the value of programmed stimulation in 205 asymptomatic patients who had had an acute myocardial infarction greater than 1 month before study. Inclusion was based on 24-hour Holter monitoring during which patients had to manifest greater than or equal to 3 consecutive ventricular beats at a rate greater than 135 beats/min. Forty-seven (23%) patients had normal, 70 (34%) mildly impaired and 88 (43%) severely impaired left ventricular function. Programmed stimulation, using up to 3 extrastimuli, was used in each. Seventy-five patients (36%) were noninducible, 59 (29%) had nonsustained VT (less than 30 seconds), 67 (33%) had sustained monomorphic VT and 4 (2%) had either polymorphic VT or ventricular fibrillation. Eighty-two patients were not treated with antiarrhythmic drugs, 57 others were placed on a program selected empirically and 66 had therapy guided by electrophysiologic testing. Satisfactory follow-up information was gathered in 187 of the 205 patients, with a mean follow-up of 18 months. One hundred forty-two patients are alive and well, 39 had sustained VT or sudden death and 6 others had a cardiac death. Only left ventricular function discriminated those who had a sustained arrhythmia or died from those who did not. Thus, programmed stimulation did not have independent predictive value in patients with nonsustained VT. However, definitive conclusions can be reached only with a large prospective study carried out in untreated patients.

Pacemaker-mediated tachycardia from a single chamber temperature sensitive pacemaker.

This report describes a case of pacemaker-mediated tachycardia from a single chamber temperature sensitive rate modulated pacemaker. The patient experienced diaphragmatic pacing that produced an increase in right ventricular blood temperature. This temperature increase was sensed by the pacemaker and led to sustained upper rate limit pacing. Decreasing the ventricular output to prevent diaphragmatic capture eliminated further episodes of pacemaker-mediated tachycardia.