James V. Talano

A possible mechanism for neurologic ischemic events in patients with atrial septal aneurysm

Abstract A trial septal aneurysm (ASA) is a congenital malformation of the atrial septum that has been associated, among other conditions, with transient ischemic attacks and strokes. 1–5 The nature of this relation is unclear. Embolic events have been attributed to thrombus formation in or at the base of the aneurysmal sac. 5,6 However, the possibility of an associated functionally patent foramen ovale leading to a paradoxical embolus from a right-to-left shunting also has been suggested. 2–4 To help clarify this issue, we analyzed the morphologic and functional characteristics of the atrial septum in patients with ASA by the use of transesophageal contrast echocardiography.

Functional chiral asymmetry in descending thoracic aorta.

To determine whether rotational blood flow or chiral asymmetry exists in the human descending thoracic aorta, we established the ability of color Doppler ultrasound to detect rotational flow in a tornado tube model of a vortex descending fluid column. In a model of the human aortic arch with a pulse duplicator, color Doppler was then used to demonstrate that rotational flow occurs first in the transverse arch and then in the proximal descending thoracic aorta. With the use of color Doppler esophageal echocardiography, 53 patients (age range, 25-78 years; mean age, 56.4 years) were prospectively examined for rotational flow in the descending thoracic aorta. At 10 cm superior to retro-left ventricular position, 22 of 38 patients (58%) revealed rotational flow with obvious diastolic counterclockwise rotation but less obvious systolic clockwise rotation. At 5 cm superior to retro-left ventricular position, 29 of 46 patients (63%) revealed rotational flow with a tendency toward systolic clockwise and diastolic counterclockwise rotation. At the retro-left ventricular position, 47 of 53 patients (89%) revealed rotational flow, usually of a clockwise direction, occurring in systole. Our data suggest that aortic flow is not purely pulsatile and axial but has a rotational component. Rotational flow begins in the aortic arch and is carried through to the descending thoracic aorta, where flow is chirally asymmetric with systolic clockwise and diastolic counterclockwise components. These data demonstrate an aortic rotational flow component that may have physiological implications for organ perfusion.

Torsade de pointes induced by N-acetylprocainamide.

N-Acetylprocainamide (NAPA), a class III antiarrhythmic drug, caused torsade de pointes in a 72 year old woman who had this arrhythmia on two previous occasions while being treated with quinidine and disopyramide. Initial evaluation with an intravenous infusion of NAPA indicated a favorable antiarrhythmic response. The QTC interval was prolonged, but the 2.4 ms/microgram per ml incremental QTC interval lengthening caused by NAPA was not greater than usual. During subsequent oral therapy with NAPA, torsade de pointes developed at plasma levels of this drug that appeared to be well tolerated during the initial evaluation.

Acquired cyanotic heart disease secondary to traumatic tricuspid regurgitation: Case report with a review of the literature

A case of traumatic tricuspid insufficiency leading to right atrial enlargement and to a patent foramen ovale with right to left shunting is presented. Six similar cases previously reported are reviewed. The time course of clinical deterioration was related to the type of tricuspid valve damage incurred. Papillary muscle rupture led to surgery within a year, whereas less severe chordal damage allowed a more benign course that lasted from 10 to 25 years from the time of injury to the time of surgery. Surgical repair of the incompetent tricuspid valve and closure of the atrial septal defect led to significant improvement. The diagnostic usefulness of radionuclide imaging and echocardiography is demonstrated in this case. A mechanism of right to left interatrial shunting in the presence of normal pulmonary arterial pressures is proposed; this invokes phasic increases in right atrial pressure from tricuspid insufficiency and streaming of blood from the inferior vena cava into the left atrium across a patent foramen ovale in a manner that resembles conditions in the fetal circulation.

Comparison of transesophageal and transthoracic echocardiography for diagnosis of right-sided cardiac lesions

Abstract Two-dimensional transthoracic echocardiography (TTE) is an established method for the evaluation of cardiac or paracardiac structural abnormalities such as tumors, vegetations and thrombi. 1–4 Cardiac structural resolution can be limited with TTE owing to anatomic interference. With transesophageal echocardiography (TEE), regions of the heart previously difficult to visualize are now readily studied. These regions include the vena cavae, right ventricular outflow tract, pulmonic valve and pulmonary trunk. The usefulness of TEE as compared with TTE in assessing right-sided cardiac pathology has not been clearly determined. We compared both techniques with the objectives of studying their diagnostic ability for the evaluation of right-sided cardiac lesions, and comparing data obtained with those from other confirmatory techniques.

Slow Channel Calcium Antagonists in the Treatment of Supraventricular Tachycardia

D EPOLARIZATION in most cardiac cells as well as skeletal muscle, and nerve cells results from increased permeability of sodium ions through a fast channel.’ An alternate mechanism appears to be operating in specialized tissue within the heart, such as the sinoatrial (SA) and atrioventricular (AV) nodes, certain nerve fibers, and smooth muscle cells where increases in membrane permeability result from opening of channels to calcium ions.* The calcium or slow channel differs from its sodium or fast channel counterpart in that its gates open and close more slowly with a resultant lowered transmembrane current carried during depolarization.3 The slow calcium channel has been implicated in the chronotropic, dromotropic, and inotropic activity of the heart as well as vascular smooth muscle contraction in coronary and systemic arterioles.3 It has also been implicated in slow pathway depolarization, characteristic of reentrant supraventricular tachyarrhythmiasP Therapeutically, calcium channel antagonists are used to depress these specific cardiac activities and inhibit coronary and systemic arteriolar smooth muscle contraction. It is their negative chronotropic and dromotropic effects that make them useful in the treatment of supraventricular tachyarrhythmias. However, the variable and numerous vascular and hemodynamic effects of this new class of agents must be considered in selecting the proper drug for the treatment of supraventricular tachyarrhythmias. The specific electrophysiologic effects that lend calcium channel antagonists effective in the treatment of supraventricular arrhythmias are their ability to (1) decrease the spontaneous rate and conduction of the sinus node; (2) prolong AV nodal conduction; and (3) lengthen the functional and effective refractory period of the AV node during AV nodal conduction and to a lesser extent during VA nodal conduction.4 The cardiac structures that are “slow” channel dependent and the electrophysiologic, electrocardiographic, hemodynamic, and vascular effects of calcium channel antagonists on these structures are listed in Table 1.

Systolic anterior motion in the absence of asymmetric septal hypertrophy. A buckling phenomenon of the chordae tendineae.

SUMMARY Systolic anterior motion (SAM) of the mitral valve in the absence of asymmetric septal hypertrophy or concentric left ventricular hypertrophy has been reported in several conditions. In this report we describe the clinical and echocardiographic findings in 15 patients who demonstrated SAM without associated organic heart disease (group 1, 10 patients) or in association with mitral valve prolapse (group 2, five patients). Cross-sectional echocardiography revealed the etiology of SAM in both groups to be early systolic anterior angular motion (“buckling”) of mitral chordal structures, rather than movement of the body of the anterior mitral leaflet into the left ventricular outflow tract. In contrast to normal subjects and group 1, group 2 patients had auscultatory evidence of mitral prolapse, a slightly greater mean left ventricular ejection fraction (p < 0.05) (normals, 69 ± 5.2%, group 1, 72 ± 3.8%, group 2, 75 ± 5.6%), and a greater mean diastolic mitral valve (D-E) excursion (p < 0.05) (normals, 1.8 ± 0.2 cm, group 1, 2.2 ± 0.3 cm, and group 2, 2.6 ± 0.4 cm). This spectrum of mitral excursion and left ventricular ejection fraction supports the concept that the mitral valve prolapse syndrome may have as its basis a mitral valve abnormality and/or a hyperdynamic state that predispose to both chordal buckling and mitral leaflet prolapse.

Frequency of pericardial effusion as determined by M-mode echocardiography in acute myocardial infarction

A pericardial friction rub occurs in 6 to 16% of patients after acute myocardial infarction (AMI), but the incidence of pericardial effusion (PE) is not known. M-mode echocardiography was done 1, 3 and 5 days after AMI in 43 consecutive patients admitted within 24 hours of AMI, and PE was detected in 16 (37%). The PE was small in 7 patients, moderate in 6 and large in 3. A pericardial friction rub developed in 8 (19%), of whom only 4 had PE. Pleuritic chest pain diminished by sitting up and relieved by antiinflammatory agents developed in 12 (28%), of whom only 5 had PE. The peak creatine kinase level was significantly higher in patients with PE (1,769 +/- 1,003 U) than in those without (1,181 +/- 838 units). More patients with PE were in Killip classification II, III or IV (11 of 16 [69%] vs 9 of 27 [33%]). The presence of PE was not associated with age, site of AMI, development of Q waves, use of heparin or previous AMI. In conclusion, PE as detected by M-mode echocardiography is frequently present after AMI, and its presence is not closely associated with the occurrence of a pericardial friction rub or typical pericardial pain.

Transesophageal echocardiography in the awake elderly patient: Its role in the clinical decision-making process

To assess the impact on the management and safety of transesophageal echocardiography (TEE) in the elderly population, the results and limitations of this technique were retrospectively analyzed in 88 patients. TEE was indicated whenever the transthoracic approach was not diagnostic or was inconsistent with the clinical setting. The most frequent clinical indications were to investigate the source of emboli, assess valvular regurgitation, and identify valvular vegetations. In 72 patients (82%) TEE significantly influenced management decisions. In selected patients TEE avoided the use of more invasive diagnostic procedures. Adverse effects included occasional premature atrial or ventricular beats (11 patients), sinus bradycardia (six patients), and protracted nausea (one patient). We conclude that in elderly patients with cardiovascular diseases, TEE plays a significant role in the decision-making process without adding a significant risk.

T wave changes consistent with epicardial involvement in acute myocardial infarction: Observations in patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis☆

OBJECTIVES This study was designed to evaluate the presence or absence of atypical T wave evolution in patients with a postinfarction pericardial effusion but without clinically recognized postinfarction pericarditis. A second purpose was to evaluate the frequency of atypical T wave evolution in a previous study of postinfarction pericarditis. BACKGROUND Electrocardiographic (ECG) criteria involving the evolution of the T wave after an acute myocardial infarction were recently described in patients with regional postinfarction pericarditis. Atypical T wave evolution was found to have a sensitivity of 100% and a specificity of 77% for clinically recognized regional postinfarction pericarditis with or without a pericardial effusion. METHODS The hospital records and serial ECGs of 20 patients with clinically recognized postinfarction pericarditis (Group I) were reviewed. The records and serial ECGs of 20 additional patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis (Group II) were also examined. The type of postinfarction T wave pattern, typical or atypical, was recorded in both groups. RESULTS All 20 patients in Group I had atypical T wave evolution. Among the 20 patients in Group II, every patient also had atypical T wave evolution. Fifteen percent of all 40 patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred postinfarction pericarditis. CONCLUSIONS The high sensitivity of atypical T wave evolution in diagnosing regional postinfarction pericarditis was confirmed. However, similar T wave alterations were also observed when a postinfarction pericardial effusion existed in the absence of clinically recognized pericarditis. Fifteen percent of patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred pericardial involvement. Thus, the presence of atypical T wave evolution may be a more sensitive indicator of a transmural infarction than the development of a Q wave.