Philip Varriale

Single‐Lead VDD Pacing System

A single pass ventricular lead with a dual chamber electrode system, designed for VDD pacing, was implanted in 17 patients (11 men, 6 women, aged 53 to 86 years, mean 74) for symptomatic bradycardia due to second‐or third‐degree AV block and normal sinus node function. Bipolar atrial electrodes, diagonally displaced along the lead axis and positioned within the right atrial cavity, are used to detect atrial activity that is then differentially processed within the pacemaker, P wave amplitude (amp) derived from a PSA‐DAA device at implant was 1.38 ± 0.28 mV. P wave signal amp derived from telemetered atrial electrograms was 1,29 ± 0.22 mV at predischarge (n = 17), 1.32 ± 0.24 mV at 3 months (n = 15), 1.30 ± 0.24 mVat 6 months (n =8), 1.51 ± 0.34 mVat 9 months (n = 4), and 1.35 ± 0.35 mV at 12 months (n = 2); and the far‐field QRS signal measured at predischarge was of negligible voltage (0.17 ± 0.07 mV). The susceptibility of the atrial sensor system to interference was noted with chest wall stimulation and only at higher sensitivities (0.1 to 0.3 mV) and not with isometric arm exercise. Intact VDD pacing function at rest and during exercise was established using Holter and periodic ECG monitoring. Postoperative complications included one lead displacement and one pocket hematoma. Three patients died postimplant of causes unrelated to pacemaker function. Advantages of the single‐lead VDD pacing include: (1) elimination of second atrial sensing lead; (2) superior atrial sensing performance; (3) effective resistance to myopotential and far‐field signal interference; and (4) stability of postimplant atrial signal amplitude.

Pacemaker Wenckebach secondary to variable latency: an unusual form of hyperkalemic pacemaker exit block.

Our present study indicates that sinus or paranodal and not ventricular tachycardia was inducible, presumably facilitated by intrinsic cellular derangements, which in this child were most expressed in the sinus region. The fact that ventricular tachycardia was not inducible at EP study suggests that the mechanism is an automatic focus (or foci) in the ventricle(s). Sinus entrance block as well as the inconsistent rate response to decremental atria1 pacing make a definite distinction between triggered and reentrant sinus tachycardia difficult. Although seemingly paradoxical, stabilization of the bidirectional tachycardia to a bigeminal rhythm following metaproterenol administration indicates a potential treatment regimen that incorporates improvement both of the muscle paralysis and ventricular dysrhythmias associated with this disorder.

Acute myocardial infarction associated with anabolic steroids in a young HIV-infected patient.

The use and abuse of anabolic‐androgenic steroids have increased over the past decade and pose a medical and public health problem. In addition to their use by athletes to increase muscle mass and improve performance, people with wasting and malignant diseases are finding that the agents improve both their physical appearance and strength. Unfortunately, anabolic steroids are associated with a number of adverse effects, not the least of which is acute myocardial infarction, which occurred in a 39‐year‐old man with human immunodeficiency virus infection. It is important for clinicians to be aware of the association and to counsel patients carefully about this and other untoward effects that may occur with the agents.

Unipolar Ventricular Electrogram in the Diagnosis of Right Ventricular Ischemic Injury

Unipolar ventricular electrograms were recorded in the right ventricular apical area in five patients with clinical, hemodynamic features of the right ventricular infarction.

Ibutilide for termination of atrial fibrillation in the Wolff-Parkinson-White syndrome.

Ibutilide promptly restored sinus rhythm on two occasions in an elderly patient with AF and rapid ventricular response associated with the WPW syndrome. As a selective Class III antiarrhythmic agent that prolongs cardiac refractoriness, ibutilide offers an alternative effective therapy for rapid termination of AF in WPW.

Short‐Term Intravenous Milrinone for Severe Congestive Heart Failure: The Good, Bad, and Not so Good

We evaluated the overall hemodynamic and clinical effects, beneficial and deleterious, of short‐term intravenous milrinone in the management of severe congestive heart failure (CHF). Numerous hemodynamic measurements were obtained in 24 patients (mean age 65 yrs) with advanced, severe CHF (New York Heart Association class IV, ejection fraction 24 ± 5%), including 3 with concomitant clinical sepsis. Hemodynamic data were recorded at baseline and after a bolus of intravenous milrinone 50 μg/kg and maintenance infusion based on creatinine clearance at 0.5, 3, 24 and 48 hours. Cardiac index increased and pulmonary capillary wedge pressure decreased significantly (p<0.001; 2.07 ± 0.36 to 3.6 ± 0.36 L/min/m2 and 20.6 ± 4.0 to 13.5 ± 2.8 mm Hg, respectively) in 24 patients 0.5 hour after initiation of therapy. These favorable hemodynamic responses, including significant decreases in systemic vascular resistance index and right atrial pressure, were sustained throughout the 48‐hour study in 19 patients (79%). Severe hypotension occurred in three patients with superimposed sepsis as the result of exaggerated vasodilatation. One patient had recurrent ventricular tachycardia and another tolerance to milrinone. In two patients, excessive decline in preload and fall in cardiac index were reversed with volume expansion. Intravenous milrinone offered significant short‐term hemodynamic benefits in most patients with severe CHF.

Hemodynamic resistance to intravenous nitroglycerin in severe congestive heart failure and restored response after diuresis

A wide variety of organic nitrate preparations are often used in the management of congestive heart failure (CHF). This class of drugs exerts a vasodilatory action, predominantly on the venous capacitance vessels, that leads to a reduced ventricular filling pressure and usually without an increase in cardiac output. 1,2 Two major problems exist that deter its widespread acceptance as an effective drug in CHF: the development of tolerance and hemodynamic resistance or primary drug failure. Tolerance is responsible for the loss of hemodynamic and clinical benefits after nitrate therapy has been initiated.3–5 An absent or feeble hemodynamic response to nitrates, a relatively common occurrence, has been reported to occur in approximately ≥50% of treated patients.6,7 However, nitrate resistance is not always apparent when intravenous nitroglycerin is used without hemodynamic monitoring. This study was designed for 2 purposes: (1) to substantiate previously described hemodynamic and clinical correlates of CHF predictive of resistance to intravenous nitroglycerin,6,7 and (2) to determine whether hemodynamic modification using alternate drug therapy might restore responsiveness to nitroglycerin.

Atrial Flutter Secondary to Hypokalemia

Electrophysiologic studies support significant hypokalemia as a cause of atrial flutter in a patient without manifest heart disease. Atrial flutter, reproducibly initiated and terminated by rapid atrial pacing during hypokalemia, was not inducible after potassium correction. In an individual with existing atrial conduction disease, hypokalemia may generate both non‐uniform atrial refractoriness and atrial premature beats, and it may facilitate the development of atrial flutter as a re‐entrant arrhythmia.