Philip Samet

Significance of the Sinus-Node Recovery Time

The phenomenon of postpacing depression of cardiac pacemakers was utilized to evaluate the sinus-node function in 56 patients by analyzing the sinus-node recovery time (SRT), that is, the interval between the last paced P wave and the following sinus P wave. Corrected SRT (CSRT) is defined as the recovery interval in excess of the sinus cycle (SRT — sinus cycle length). The SRT was measured following sinus-node suppression by (1) isolated premature beats (PABs) and (2) atrial pacing (AP) at rates of 100 to 140/min for periods of 2 to 5 min at each level. Twenty-eight patients had normal heart rates (group A), and 28 patients had sinus bradycardia (SB; group B). Ten of the 28 patients with SB were restudied after receiving atropine (2 mg intravenously). The CSRT with PABs was similar in both group A and group B patients and remained essentially unchanged after atropine despite a decrease in sinus cycle length. The phenomenon of interpolated PABs was demonstrated in seven of the 56 patients. In 27 of the 28 patients with normal heart rates (group A), the CSRT with AP ranged from 110 to 525 msec and was essentially independent of the rate and duration of AP. In the remaining one patient of group A, despite a normal heart rate, the CSRT was prolonged (1810 msec) and directly dependent on the rate and duration of AP. In 12 of the 28 patients with SB, the CSRT was comparable to that in group A (≦525 msec). In the remaining 16 patients with SB (group B), the CSRT ranged from 560 to 3740 msec and was usually directly proportional to the rate and duration of AP. After atropine in most of the patients with a prolonged CSRT, the CSRT remained abnormal whereas in others junctional escape beats appeared first, followed eventually by normal sinus rhythm. In a single patient with SB and an abnormal CSRT, restudy 7½ months later again showed a prolonged CSRT indicating the reproducibility of the measurement. The CSRT with AP provides a potentially useful clinical means of assessing the sinus-node function and thereby aids in the diagnosis of the “sick sinus syndrome.’ It is stressed that AP was found to be more reliable than PABs in eliciting an abnormal response. Furthermore, a normal sinus (atrial) rate does not necessarily provide assurance of a normal sinus-node response to AP, that is, normal sinus-node function.

Hemodynamic sequelae of atrial, ventricular, and sequential atrioventricular pacing in cardiac patients

Abstract Comparison of the effects of atrial, ventricular, and sequential atrioventricular pacing in a group of patients with rheumatic heart disease and in a group with pulmonary emphysema has demonstrated that the absence of synchronized atrioventricular activity rather than aberrant ventricular depolarization is primarily responsible for the hemodynamic difference between atrial and ventricular pacing.

Selective In Situ Parasympathetic Control of the Canine Sinoatrial and Atrioventricular Nodes

Methods were devised for the selective alteration of parasympathetic control over the sinoatrial (SA) or the atrioventricular (AV) node in anesthetized, thoracotomized mongrel dogs. Two epicardial sites were located at which parasympathetic nerve fibers enroute to the SA or the AV node could be stimulated or blocked. Selective nerve stimulation was accomplished with brief pulses (0.05 msec), and blockade was accomplished with topically applied lidocaine. At the intercaval site, only the SA node was affected. At the site near the coronary sinus ostium, only the AV node was affected in terms of parasympathetic control, but sometimes there were modest sympathetic effects on the SA node. The effects of stimulation at these sites, except for the SA speeding produced by stimulation at the site near the coronary sinus, were blocked by atropine. The effects were also blocked by ganglionic blockade. Probably, preganglionic parasympathetic fibers to the nodes are concentrated at these sites.

Atrial contribution to cardiac output in complete heart block

Abstract Cardiac output studies were performed in 6 patients with complete heart block during four kinds of ventricular rhythm. These include ventricular or His-bundle pacing at the control rate, right ventricular outflow tract catheter electrode pacing, and both synchronous and atrial synchronous pacing by means of a Cordis Synchrocor unit. The latter two rhythms are defined as those with P wave, ventricular stimulus and QRS complex sequences, and atrial stimulus, P wave, ventricular stimulus and QRS complex sequences, respectively. Thirty-four paired observations were made during equal atrial and ventricular pacing rates in these patients. The importance of atrial systole for maintenance of cardiac output is clearly demonstrated by these data.

Significance of the atrial contribution to ventricular filling

Abstract The contributions of atrial systole to ventricular filling are emphasized by analyses of pressure curve data in (1) patients with complete heart block studied by right and left heart catheterization, (2) patients with sinus rhythm and atrial fibrillation and (3) sinus rhythm and ventricular premature beats. The level of systolic and diastolic right and left heart pressures varies with the temporal relation between the P and QRS complexes in patients with complete heart block. Peak pressures are recorded when there is a normal temporal relation between the P and QRS complexes. The rate of rise of the systemic arterial pressure curve is also at a maximum when the normal P-QRS relation is maintained. Comparison of left ventricular and systemic arterial pressures during sinus rhythm and ventricular premature beats demonstrates higher systolic peak pressures during sinus rhythm with normal atrioventricular conduction; of equal importance is the observation that left ventricular end-diastolic pressures are higher during sinus rhythm than during a series of ventricular premature beats. One subject was studied during both atrial fibrillation and normal sinus rhythm in the course of left heart catheterization. Left ventricular. systolic and end-diastolic pressures were higher during normal sinus rhythm than during atrial fibrillation. The development of mitral regurgitation during ectopic ventricular beats is also illustrated. These data demonstrate the physiologic importance of maintaining the normal temporal sequence of atrioventricular activity.

Hemodynamic consequences of sequential atrioventricular pacing. Subjects with normal hearts.

Abstract The hemodynamic sequelae of sequential atrioventricular pacing were compared to those of atrial and ventricular pacing and analyzed. The results clearly demonstrate that aberrant ventricular depolarization per se is of relatively minor hemodynamic import but that sequential atrial and ventricular activity is essential for optimal ventricular function even in the normal subject.

Treatment of Supraventricular Tachycardias by Rapid Atrial Stimulation

In 10 patients, 24 episodes of supraventricular tachycardia were treated by rapid electrical stimulation of the right atrium. One episode of sinus tachycardia, eight episodes of atrial tachycardia, two episodes of atrial flutter, and 13 episodes of A-V junctional tachycardia occurred. In each case the diagnosis of the arrhythmia was documented by obtaining unipolar and bipolar intra-atrial electrograms.In three cases of supraventricular tachycardia the ventricular rate was slowed as a result of an increased atrial rate. The increased atrial rate caused an increase of the functional refractory period of the A-V junction, and thus, fewer atrial impulses were transmitted to the ventricles.In seven cases, 21 episodes of supraventricular tachycardia were terminated by rapid atrial stimulation. In six of these cases the tachycardia was converted to normal sinus rhythm either during or shortly after atrial stimulation. In one case, 12 episodes of A-V junctional tachycardia were converted to rhythms varying between normal sinus rhythm and a slow A-V junctional rhythm. In this case, after termination of the last episode of A-V junctional tachycardia, the rhythm was stabilized by atrial pacing.

Hemodynamic Sequelae of Cardiac Arrhythmias

The hemodynamic consequences of cardiac arrhythmias depend on various factors, including the ventricular rate and the duration of the abnormal rate, the temporal relationship between atrial and ventricular activity, the sequence of ventricular activation, the functional state of the heart, the irregularity of the cycle length, associated drug therapy, the peripheral vascular vasomotor system, disease in organ systems other than the heart, and the degree of anxiety caused by the disease processes. Sinus bradycardia, even with rates as low as 40 beats/min, may not be associated with significant hemodynamic consequences unless the stroke volume is limited by myocardial or valvular disease, as in acute myocardial infarction. Cardiac output usually, but not invariably, falls when atrial fibrillation replaces normal sinus rhythm, even at comparable ventricular rates, both at rest and during exercise. Similar observations have been made during the development of atrial flutter despite the persistence of effective mechanical atrial activity in at least some cases. Marked hemodynamic changes are frequent in the course of ventricular tachycardia with systemic arterial hypotension, a decrease in cardiac output, and evidence of cerebral, coronary, and renal vascular insufficiency. Cyclic variations in systemic and pulmonary arterial pressures are common during atrioventricular dissociation. Cardiac output is generally depressed during the severe bradycardia of acquired complete heart block with evidence of atrioventricular valvular insufficiency. Increase of the heart rate by ventricular pacing reverses all or some of these abnormalities. The changes in congenital complete heart block are considerably less severe because myocardial insufficiency is less frequently seen in congenital complete heart block.

Thrombosis on Bjork-Shiley aortic valve prosthesis: Clinical, arteriographic, echocardiographic and therapeutic observations in seven cases

Abstract Seven patients with massive thrombosis on a Bjork-Shiley aortic valve prosthesis are described. This complication was documented in 5 percent of our patients with a Bjork-Shiley valve and occurred 3 to 19 months (mean 13 months) after insertion of the prosthesis. Only one patient had adequate anticoagulant therapy at the time of diagnosis. All patients had acute or subacute clinical deterioration. Anginal chest pain was the presenting symptom in four patients, and acute left ventricular failure in three. In all patients, the closing click of the Bjork-Shiley prosthesis was not heard, and new aortic systolic or diastolic murmurs were audible. Cardiac catheterization and aortic root cinearteriography were performed in five patients. Severe prosthetic regurgitation was found In four patients and mild regurgitation in one. Abnormal disc motion—fixation of the disc in the open position, abnormal limited opening of the disc or imperfect closure—was demonstrated in all arteriographic studies. Echocardiograms revealed an immobile disc in two patients. Five patients were surgically treated by thrombectomy and debridement of the prosthetic valve; the original prostheses were left in situ. Four of these patients are alive and one died. Two patients who did not undergo surgical treatment died. Thrombosis on the Bjork-Shiley aortic valve has a high fatality rate. Suspicion of this complication should be followed by emergency catheterization and surgery. In critically ill patients, surgery may be required even without angiography. The occurrence of this serious complication, mostly in patients with a normal coagulatory state, indicates the need for permanent anticoagulation in patients with a Bjork-Shiley aortic valve prosthesis.

Myocardial dysfunction associated with valvular heart disease

Abstract Seventy-one patients undergoing valve replacement surgery were studied before and after operation to determine change of clinical condition and ventricular contractility. Preoperatively, all patients had functional class III or IV disease (New York Heart Association classification) and 55 percent had myocardial dysfunction. Post-operatively, the condition of 86 percent of patients improved clinically by at least 1 functional class, but 56 percent of patients had myocardial dysfunction. Cardiac index and left ventricular end-diastolic pressures were closely related to changes in angiographically determined myocardial contractility. Neither patient age, sex, duration of cardiopulmonary bypass, residual uncorrected valve disease nor coronary artery disease alone determined the degree of impairment in left ventricular contractility. A high incidence of myocardial dysfunction was found pre- and postoperatively in this study. In 16 patients with pure mitral stenosis, 6 (38 percent) had left ventricular dysfunction preoperatively, demonstrating intrinsic myocardial disease, possibly chronic rheumatic myocarditis. The demonstration of postoperative myocardial contractile abnormalities in previously normal patients suggests an intraoperative cause, perhaps related to cardiopulmonary bypass. Postoperative dysfunction may (1) exist preoperatively and remain unchanged, (2) occur intraoperatively, or (3) exist in a latent form preoperatively but be aggravated by the stress of surgery. Without both pre- and postoperative microscopic examination of the myocardium in the same patient, it is impossible to determine which process is primary.