Discrimination of ventricular tachycardia from sinus tachycardia and atrial fibrillation in a tiered-therapy cardioverter-defibrillator.

OBJECTIVES: This study was conducted to evaluate criteria for discrimination of ventricular tachycardia from atrial fibrillation and sinus tachycardia in a tiered-therapy cardioverter-defibrillator (Medtronic PCD). BACKGROUND: Interval stability algorithms discriminate ventricular tachycardia from atrial fibrillation. Onset algorithms discriminate ventricular tachycardia from sinus tachycardia. Neither has been validated clinically. METHODS: The stability criterion requires that a ventricular tachycardia interval not vary from any of the three previous intervals by more than the programmable stability value. The onset criterion detects initiation of ventricular tachycardia only if the ratio of an interval to the mean of four previous intervals is less than a programmed onset ratio and either the second or third preceding interval exceeds the ventricular tachycardia detection interval. We evaluated these criteria in 100 patients at electrophysiologic study and exercise testing (65 patients) and during a mean (+/- SD) follow-up of 16.2 +/- 7.9 months. The PCDs were programmed to tiered therapy in 54 patients. In the remaining 46 patients, the PCD's memory for detected ventricular tachycardia was used to study the specificity of the chosen onset criterion for rejecting sinus tachycardia. We used stored intervals preceding appropriate (n = 99) and inappropriate (n = 54) detections to test a new onset criterion that was less sensitive to a single index interval. RESULTS: Programmed stability of 40 ms decreased detection of induced atrial fibrillation by 95% (20 patients), paroxysmal atrial fibrillation by 95% (6 patients) and chronic atrial fibrillation by 99% (9 patients); all episodes of spontaneous (n = 877) and induced (n = 339) ventricular tachycardia were detected. A programmed onset ratio of 87% rejected sinus acceleration (98%) but caused underdetection of 0.5% of ventricular tachycardias. The onset criterion permitted inappropriate detection of premature ventricular complexes during sinus tachycardia, but the new criterion reduced these inappropriate detections by 98%. CONCLUSIONS: The PCD's onset and stability criteria reduced inappropriate detection of atrial fibrillation and sinus acceleration while detecting 99.5% of ventricular tachycardias.

Role of the pericardium in the regulation of myocardial blood flow and its distribution in the normal and acutely failing left ventricle of the dog.

The effects of the pericardium on the amount and distribution of left ventricular myocardial blood flow were studied. In 10 normal dogs, transfusion of blood from a donor dog resulted in modest increases in coronary flow and ventricular diameter that were greater with an open than a closed pericardium. The ratio of subendocardial to subepicardial flow remained normal with or without the pericardium, at low and high diastolic ventricular pressure, and before and after pharmacological vasodilation with chromonar. In 18 dogs, cardiac failure was induced by constant infusion of the metabolic inhibitor, phenformin. Modest ventricular dilatation occurred if the pericardium was open. A progressive rise in myocardial blood flow developed in those with the pericardium open (1.06 rising to 3.02 ml . g-1 . min-1). A lesser increase (0.62 to 1.75 ml . g-1 . min-1) was seen in dogs with the pericardium closed; they selectively increased subendocardial flow, producing an average subendocardial to subepicardial flow ratio of 2.25. Pharmacological vasodilatation then resulted in uniform transmural flow. The pericardium can influence myocardial flow indirectly by influencing myocardial metabolic demand, when the heart is stressed. It may have a beneficial role in preventing the increased oxygen and coronary flow requirements produced by ventricular dilatation.

Interrupted aortic arch: factors influencing prognosis.

From January, 1969, to June, 1974, 11 infants with interrupted aortic arch were operated upon. Eight of them died in the perioperative period. Their cases were reviewed in an attempt to find factors influencing the prognosis. Age, weight, preoperative hemodynamics, angiographic findings, and the type of arch anomaly did not influence the outcome. The operation, whether palliative or involving intracardiac repair, did not affect the prognosis. The only factor related to the outcome was the size of the conduit: in all infants who died, the vessel used to bridge the gap (carotid or subclavian artery) was of narrow diameter. In the 3 patients who survived it was of much larger bore. We conclude that in the repair of interrupted aortic arch, an adequate conduit is essential for success.

Sudden hemolysis indicating prosthetic valve dysfunction.

Ten months after aortic valve replacement (Björk-Shiley prosthesis) a 57-year-old man had thrombotic encapsulation of his prosthetic valve. The only clinical manifestation of this serious complication was gross hemoglobinuria. The management of the patient is described. The slightest change in the condition of a patient after prosthetic valve replacement should be viewed as a possible sign of thrombosis.

Valvar subcoronary aortic stenosis in dogs.

A technique for producing valvar aortic stenosis is described. The noncoronary sinus of Valsalva is plicated externally at a level proximal to the origin of the coronary arteries. The major intraoperative problems are hemorrhage, acute left ventricular failure, and heart block, all of which can be avoided. The survival rate in 26 dogs was 54% and all the survivors remained active. Moderate left ventricular hypertrophy was produced.

Myocardial infarction after aortocoronary bypass: etiologic factors.

To ascertain the frequency and probable determinants of myocardial infarction after aortocoronary bypass, two groups of patients were studied: a group of 20 patients who underwent valve replacement of repair of congenital anomalies and a group of 24 patients who underwent aortocoronary bypass. Postoperative myocardial infarction was diagnosed by an increase in serum creatine phosphokinase concentration to a minimum of 1200 IU in two consecutive samples. The frequency of myocardial infarction differed between the groups, being only 5% in group 1 but 20.4% in group 2. In the patients undergoing coronary artery surgery, the duration of bypass, the aortic cross-clamp time and the vent site did not influence the rate of infarction. However, the incidence of myocardial necrosis did correlate with the number of vessels bypassed. In no case was the clinical course influenced by the infarction. Our results suggest that the frequency of perioperative infarction is higher in coronary artery surgery than in other adult cardiac surgery, and that the most important determining factor is the number of diseased vessels.

Coronary blood flow in experimental canine left ventricular hypertrophy.

To determine whether left ventricular hypertrophy [LVH] altered total and regional coronary blood flow, we inflated a balloon around the ascending aorta of nine dogs; six acute and six sham-operated dogs were controls. After 6 weeks, all dogs were studied with an open chest under anesthesia; the balloons were deflated. There was moderate LVH as shown by increased left ventricular weight and fiber diameter. At rest there were no major differences of coronary flow or resistance per gram of muscle. With maximal coronary vasodilation due to adenosine or carbochrome, mean coronary vascular resistance was 84% higher in LVH than in normal hearts; with isoproterenol, resistance was 54% higher in LVH. These changes were similar in right and left ventricles. Minimal coronary resistance at end diastole also was higher in LVH--64% and 94% for the two sets of vasodilators, respectively. There were no significant differences in capillary or large vessel proportional volumes in LVH and control dogs, but arterial capacity could not be estimated. The raised minimal coronary resistance suggests the possibility that, with stress, coronary flow, especially to subendocardial muscle, might be inappropriate and perhaps cause ischemic damage. However, the changes noted might have been due to coronary arterial responses to raised coronary pressures rather than to hypertrophy itself.

Rapid-freezing transmural cardiac biopsy drill.

We have built a transmural cardiac biopsy drill that uses an air turbine (10,000 rpm) to turn a stainless steel bore of either 2.0 or 4.5 mm diam. Vacuum draws the cut biopsies through the drill into isopentane chilled to -150 degrees C with liquid nitrogen. The steel bores cut through the beating canine left ventricular free wall in 0.14 +/- 0.04 (SD) permitting sampling in discrete portions of the cardiac cycle. Small and large biopsies traverse the drill in 0.48 +/- 0.19 and 0.15 +/- 0.04 s, respectively. Large biopsies freeze in 1.46 +/- 0.73 s, whereas small biopsies are calculated to freeze in 0.28 s. Average biopsy weights are 34 +/- 14 and 180 +/- 71 mg. Left ventricular myocardial blood flow measured with radionuclide-labeled microspheres showed that muscle plugs sutured into wound sites of 4.5-mm-diam biopsies cause a 30% reduction in myocardial blood flow within 0.5 cm of the biopsy site. Light microscopy shows normal cardiac muscle with little damage from drill rotation.