Biomedical subjects
Publications and source records attributed to C S Kuo.
A patient with chronic renal failure who experienced symptomatic ventricular tachycardia was treated successfully with procainamide (PA) after numerous dosage adjustments to optimize his clinical response and serum PA and NAPA concentrations. Efforts to maintain total combined serum levels at 20-30 micrograms/ml led to sustained ventricular ectopy whenever the serum PA levels decreased to less than 8 micrograms/ml.
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A case with Type A Wolff-Parkinson-White pattern and recurrent sustained ventricular tachycardia is presented. Because of ventricular pre-excitation, electrocardiographic clues suggestive of ventricular tachycardia were ignored and the diagnosis of supraventricular tachycardia with conduction to the ventricles over the accessory pathway was made during each admission to the hospital. Ventricular tachycardia was suspected only when programmed stimulation studies performed twelve years after initial presentation and many hospitalizations failed to induce a tachycardia with a QRS pattern similar to that of spontaneously occurring tachycardia. The diagnosis of ventricular tachycardia was later confirmed by intracardiac recordings made during a spontaneous episode of tachycardia. Tachycardia was unresponsive to all conventional antiarrhythmic agents but was controlled with amiodarone. The differential diagnosis of wide QRS complex tachycardia in patients with Wolff-Parkinson-White syndrome, the implications of correctly diagnosing the tachycardia, and the usefulness of intracardiac electrophysiologic studies in differentiating supraventricular tachycardia with aberrant conduction from ventricular tachycardia are discussed.
Lidocaine was administered intravenously (a loading dose of 1.5 mg/kg body weight followed by a 3 mg/min infusion) to 10 patients with complete atrioventricular (A-V) block proximal to the His bundle and A-V junctional escape rhythm. A-V block was not due to an acute myocardial infarction in seven patients (group I) and was due to an acute inferior wall infarction in three patients (group II). Lidocaine had either no or only a slight depressant effect on the rate of the escape pacemaker in patients in group I but caused severe bradycardia or asystole in two of three patients in group II. Lidocaine had no consistent effect on the atrial rate and did not change the QRS duration and H-V intervals in any patient. These observations are consistent with the results of animal studies that showed that lidocaine selectively depressed conduction in ischemic or depolarized myocardium. The findings also suggest that the use of lidocaine without prior insertion of a pacemaker is unsafe in patients with acute myocardial infarction and complete A-V block proximal to the His bundle.
Morphology of ventricular ectopic complexes was examined in 1,746 ECGs of 149 patients with permanent ventricular pacemakers. In 20 of 80 patients (25%) the morphology of ventricular ectopic complexes was similar to that of the paced complex. This resulted in a ventricular couplet where the spontaneous premature complex originated at the site of pacing, possibly due to local re-entry. Repeated re-entry (two ventricular ectopic complexes in a row) occurred only in one of these patients, and none had ventricular tachycardia. These observations 1) verify the existence of a mechanism which we have postulated in explaining the association between couplets and ventricular parasystole, and 2) confirm the rare occurrence of repeated reentry in such a setting. Other observations in this studyshow that premature stimulation during right ventricular pacing may alter morphology of the ventricular complex from a left to right bundle branch block pattern in some leads.
The acute effect of verapamil on the ventricular rate in atrial fibrillation and flutter was studied in 15 patients, 13 of whom had heart rate inadequately controlled with digitalis. Plasma concentrations were measured 5 and 10 min after intravenous doses of 0.075 mg/kg and 0.15 mg/kg verapamil. In 9 patients who were clinically compensated, the 0.075-mg dose alone decreased the ventricular rate to under 100/min (responders); in the remaining 6, who had acute congestive heart failure manifested by orthopnea, rales, and pulmonary congestion, ventricular rates were above 100/min after the 0.075-mg dose (nonresponders). The 6 nonresponders received the 0.15-mg dose 30 min later. In all, the response was greater when plasma drug concentration rose after the high dose, although the rate decrease was smaller than in the 9 compensated patients who received the low dose. These results can be explained by assuming an antagonism of the verapamil effect by sympathetic stimulation in nonresponders.
In 78 consecutive patients with uniform ventricular ectopic complexes and without heart disease, ventricular couplets were present significantly more often when the coupling interval of ventricular ectopic complexes was variable than when it was fixed (P less than 0.04). In 69 consecutive patients with couplets, the prevalence of a variable coupling interval was significantly greater than that of (55 versus 14 cases; P less than 0.001). Among 55 patients with a variable coupling interval, ventricular parasystole was probable in 38 and possible in 17 patients. These results suggest that the association between ventricular couplets and parasystole is not coincidental. Of several possible mechanisms responsible for this association reentry within the parasystolic focus or its vicinity is the most probable. This may explain the observation that the couplets are seldom followed by consecutive ventricular ectopic complexes or ventricular tachycardia. If this hypothesis is correct, the clinical significance of ventricular couplets in the presence of ventricular parasystole may be similar to that of single reentrant ventricular ectopic complexes.
Myocardial injury during a variety of cardiac surgical operations was determined in 57 patients by serial electrocardiograms (ECG's), serial determinations of serum creatine phosphokinase (CPK), and perioperative and postoperative technetium-99m stannous pyrophosphate (PYP) scans. ECG evidence of injury developed in four patients, whereas positive localized injury by PYP scan developed in ten. Twenty-one patients had elevated CPK enzymes postoperatively. The localization of injury by PYP scan correlated with ECG evidence of infarction in only one of four patients. Localized left ventricular injury by PYP scan without new Q waves on the ECG was common (5/12) in patients undergoing aortic valve replacement with perfusion of the coronary arteries. The injury in patients with congenital heart disease occurred at sites of ventricular incision or suggested possible air embolization of the coronary arteries. Perioperative infarction is frequently segmental and nontransmural and occurs in patients with coronary, valvular, and congenital heart disease.
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Changes in the duration of monophasic action potentials on the anterior and posterior walls of the dog ventricle were correlated with changes in T wave polarity and duration of the Q-T interval after (1) left stellate ganglion transection, (2) right stellate ganglion stimulation, and (3) administration of isoproterenol before or after these procedures. Left stellate ganglion transection and right stellate ganglion stimulation produced similar changes in T wave polarity, but the former prolonged and the latter shortened the Q-T interval. All procedures changed the duration of the monophasic action potential and the Q-T interval in the same direction. The reversal of T wave polarity induced by left stellate ganglion transection, right stellate ganglion stimulation or administration of isoproterenol after left stellate ganglion transection was associated with an average change of 13 to 17 msec in the difference between the monophasic action potential durations on the anterior and posterior ventricular walls. Isoproterenol restored to normal the neurogenic T wave abnormalities produced by left stellate ganglion transection and right stellate ganglion stimulation. The drug shortened the previously prolonged monophasic action potential more than the normal monophasic action potential, and the normal monophasic action potential more than the previously shortened monophasic action potential. This study confirms that the T wave is a sensitive indicator of relatively small changes (less than 20 msec) in the sequence of ventricular repolarization and explains the mechanism by which isoproterenol "normalizes" the primary T wave abnormalities.
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We correlated primary T wave changes with the changes of monophasic action potentials (MAP) recorded with suction electrodes from the ventricular surface of the dog heart following systemic or intracoronary infusions of small doses of isoproterenol (ISP). The portions of the heart perfused with ISP were excised and weighed to determine the mass of perfused tissue. ISP shortened the ventricular MAP by an average of 12-18 msec in the entire ventricular mass following systemic administration, in 34 plus or minus 6 per cent of the ventricular mass after injection into the left circumflex coronary artery (LCA), in 8.5 plus or minus 2.6% of the ventricular mass after injection into a branch of LCA and in 17 plus or minus 8 per cent of the ventricular mass after injection into the right CA. The MAP changes induced by ISP were similar to the transmembrane action potential changes recorded with microelectrodes from papillary muscles excised from the same dogs. The most important results of this study showed that: 1) the early and the late effects of ISP administration produced opposite effects on the T wave polarity. The early T wave change was associated with nonhomogeneous and the late change with homogeneous MAP shortening; 2) the T wave change was greater after infusion into LCA than after systemic administration, 3) the T wave change was greater after infusion into LCA than after infusion into LCA branch apparently because of greater mass of the ISP-perfused myocardium; 4) the T wave change was greater after infusion into LCA branch than after infusion into RCA, apparently due to the unequal regional repolarization contribution to the T wave; 5) the ventricular gradient did not always reflect the magnitude of the primary T wave change. Our study helps to identify factors contributing to high sensitivity and low specificity of T wave abnormalities.
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To determine whether a semi-automatic oscillometric blood pressure (BP) monitor Dinamap 1846SX (DIN) can replace the standard mercury sphygmomanometer (SMS) for BP measurements in diabetic patients and their offspring, we compared SMS with DIN in 105 diabetic patients and their families. Their mean age was 50.6 (range 24-86) years, of whom 41 had diabetes mellitus (DM), 32 impaired glucose tolerance and 32 non-DM. After resting quietly for 10 min, their right arm BP were measured twice with each device at random and with 1-min intervals between each measurement. Agreement between measurements was tested by plotting the differences between the methods against means and by intraclass correlation coefficient (r(I)). The DIN was also evaluated by the criteria of American Association for the Advancement of Medical Instrumentation (AAMI), the British Hypertension Society (BHS) criteria and clinical criteria of O'Brien. All measurements by DIN [first readings or averaged readings of duplicate measurements of systolic BP (SBP) or diastolic BP (DBP)] satisfied the AAMI criteria and had good agreement with SMS (r(I)=. 951 for SBP and r(I)=.905 for DBP). The first readings of systolic BP measured by DIN vs. SMS failed to satisfy the criteria by O'Brien and reached BHS grade C level. Other measurements passed the limits of O'Brien and reached BHS grade A or B. In conclusion, averaged readings of duplicate BP measurements by DIN are interchangeable with that by SMS in Chinese diabetic patients and their offspring. Only one single DIN measurement is not acceptable for clinical application.
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