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Stress echocardiography is used increasingly in the evaluation of coronary artery disease. The echocardiographic evaluation of ischemia is based on stress-induced changes in wall motion and wall thickening of the ischemic segments. Studies have demonstrated that left ventricular volumetric changes may induce changes in wall thickness. The aim of the study was to evaluate whether significant changes in ventricular volume, wall thickness, and wall thickening occur during stress echocardiography with atrial pacing. Seven German Landrace female pigs were studied 4 weeks after the induction of a small myocardial infarction. Echocardiographic measurements were conducted in noninfarcted segments on the short-axis view at baseline and during atrial pacing at 120, 150, and 180 beats/min. End-diastolic circumferential area decreased from 12.3 +/- 2.0 cm2 at baseline to 8.9 +/- 1.9 cm2 at 180 beats/min of atrial pacing (p0.01). Mean wall thickness (interventricular septal plus posterior wall thickness divided by 2) increased markedly and progressively from 6.7 +/- 0.6 mm at baseline to 9.8 +/- 1.0 mm at 180 beats/min (p0.01). The increase in wall thickness correlated inversely with end-diastolic area (r = -0.57; p0.01). Percent systolic thickening decreased from 38.9 +/- 12.0 at baseline to 14.9 +/- 7.4 at 180 beats/min of atrial pacing (p0.01). The decrease in percent wall thickening correlated with the increase in wall thickness (r = -0.71; p0.01). In conclusion, this study shows that a marked increase in wall thickness (pseudohypertrophy) and decrease in percent systolic thickening are observed during rapid atrial pacing in normal myocardium and do not indicate stress-induced left ventricular dysfunction.

There is probably not one single pathologic condition that has been studied by echocardiography as extensively as pericardial effusion and cardiac tamponade. Among the many reported echocardiographic signs of cardiac tamponade, the most frequent and diagnostically useful are the following: right ventricular and right atrial diastolic collapse 1,2 ; a “swinging heart” 3 ; and phasic respiratory changes of ventricular dimensions. 4 This report describes a new echocardiographic sign, typical for pericardial effusion and tamponade, namely a transient thickening of left ventricular (LV) wall associated with cardiac tamponade.

Transesophageal echocardiography yields a highly accurate diagnosis in the detection of valvular vegetations. We describe a case in which omniplane transesophageal echocardiography failed to demonstrate a large vegetation protruding from a Starr-Edwards mitral prosthesis, toward the left ventricular outflow tract. The vegetation could be detected solely by transthoracic echocardiography.

Several studies have shown that in patients with systolic dysfunction, a restrictive left ventricular (LV) fi lling pattern (characterized on Doppler echocardiography by a shortened E-wave deceleration time, compatible with increased LV fi lling pressure) independently predicts outcome. 1–3 However, because these studies failed to include patients with relatively preserved LV function, little is known about the impact of a restrictive fi lling pattern (RFP) in this patient group. In this retrospective matched-controlled study, we assessed the prevalence of RFPs in patients with relatively preserved LV function and compared their clinical correlates with those of a group of patients matched according to their systolic LV function.

Objectives. The aim of this study was to investigate the significance of further ST elevation that occurs during the 1st h of thrombolytic therapy before the expected resolution. Background. Early resolution of ST segment elevation is commonly accepted as a marker of clinical reperfusion during thrombolytic therapy far acute myocardial infarction. Using frequent electrocardiographic recordings, we observed in some patients further ST elevation that occurred during hour 1 of thrombolysis before the expected resolution. Methods. To investigate the significance of this pattern, we classified 177 consecutive patients with a first acute myocardial infarction into two groups: Group A, 98 patients with ST elevation ≥1 mm above the initial ST elevation during the 1st h of thrombolytic therapy, and Group B, 79 patients without this finding. Results. Although the presence or absence of additional ST elevation was not associated with a clinical or prognostic difference in patients with a first inferior or posterior acute myocardial infarction, its presence indicated a more favorable clinical outcome and prognosis in patients with anterior infarction. Among the patients with anterior infarction the 65 patients in Group A had a higher ejection fraction (44 ± 9% vs. 35 ± 11%, p < 0.01), less heart failure (15% vs. 35%, p = 0.02) and 8 lower in-hospital mortality rate (0% vs. 8%, p = 0.04) than did the 37 patients from Group B. Conclusions. Additional ST elevation early during thrombolytic therapy in patients with anterior infarction suggests a favorable clinical outcome and thus may be indicative of successful reperfusion.

The dipyridamole stress test is used with thallium-201 to detect areas of inhomogeneity of blood flow that point to coronary artery disease (CAD). It is unclear whether dipyridamole produces inhomogeneous perfusion only or whether it actually decreases net flow in the obstructed vessels and produces true ischemia. It is also unclear what effect dipyridamole has on global and segmental left ventricular function. Therefore, ejection fraction, segmental wall motion and ventricular volume equivalents were measured before and after dipyridamole in 113 patients and 32 normal subjects. Ejection fraction responded in an abnormal fashion in 98 patients (87%), decreasing from 49 +/- 11% to 43 +/- 13% (p less than 0.0001), whereas it increased in 29 normal subjects (90%) from 57 +/- 6% to 64 +/- 10% (p less than 0.0001). Wall motion worsened distinctly in 75 patients (66%), and pressure/volume ratio deteriorated in 72%. The effect of dipyridamole lasted between 10 and 25 minutes, but was promptly reversed by aminophylline. These findings indicate that dipyridamole generally induces true ischemia in CAD. Furthermore, the degree of dysfunction is related to the angiographically assessed severity of CAD. The shortness of breath (seen in 10% of patients) may be partially explained by the findings, and it seems advisable to give aminophylline to every patient in order to promptly correct left ventricular dysfunction.

Percutaneous balloon valvuloplasty was recently introduced in the treatment of calcific aortic stenosis, the leading valvular disease among the elderly in the Western world [1–4]. This paper reports results with percutaneous aortic balloon valvuloplasty in a group of elderly patients with congestive heart failure.

Nitroglycerin (NTG) ointment has been shown to be effective in the treatment of angina pectoris and congestive heart failure. Its duration of action is usually 4 to 6 hours. This study presents data that show that a new slow-release NTG ointment produces hemodynamic improvement over at least 24 hours. Twenty patients with coronary artery disease were tested with serial gated equilibrium radionuclide ventriculography before and at various stages of continuous, once-a-day use of slow-release NTG ointment and 4 days after cessation of therapy. NTG ointment significantly (p less than 0.005) decreased left ventricular end-diastolic and end-systolic volumes both at rest (23% and 33%) and during handgrip exercise (22% and 32%) when examined after continuous usage of at least 24 hours. Ejection fraction increased 21% at rest, from 0.42 +/- 0.15 to 0.51 +/- -0.18, p less than 0.0005). The ratio of peak systolic pressure to end-systolic volume increased 85% at rest (p less than 0.05) and 54% during exercise (p less than 0.01). All values had returned to baseline 4 days after cessation of treatment. Thus, slow-release NTG ointment may be useful in the treatment of angina pectoris and congestive heart failure on a once-a-day basis.

Eleven patients with implanted pervenous pacemakers were found to have unusual QRS morphology resembling right bundle branch block (RBBB) on the 12-lead electrocardiogram. In nine patients, the tip of the electrode catheter was established with certainty to be in the right ventricular apex. In eight of the nine, the standard leads showed a left bundle branch block pattern (LBBB), whereas only the precordial leads V 1 and V 2 resembled RBBB. In only one of the nine was the RBBB pattern also seen in the standard leads. In all nine, recording the precordial leads one intercostal space below the usual space eliminated the RBBB pattern in V 1 -V 2 and resulted in inscription of a QS complex, whereas recording the leads one space higher than usual enhanced the height of the R wave. This is explained by the marked superior and slight anterior orientation of the main QRS complex in right ventricular pacing. It is suggested that the pattern of RBBB in V 1 -V 2 +LBBB in lead 1 be named pseudo RBBB pattern since it does not represent left prior to right ventricular activation.

In a prospective study murmurs increased in intensity with carotid sinus pressure in 18 of 26 patients with hypertrophic obstructive cardiomyopathy (HOCM) (sensitivity, 69.2 percent for the 26 patients, 85.7 percent for the 21 patients in whom heart rate and blood pressure decreased with carotid sinus pressure). On the other hand, the murmur remained constant or decreased in all but one of 104 patients with valvular aortic stenosis, mitral insufficiency, hypertrophic nonobstructive cardiomyopathy, and systolic murmurs of miscellaneous origins (specificity, 99 percent; positive predictive value, 94.7 percent). Catheterization, indirect arterial pressure tracings, and echocardiographic studies indicated that carotid sinus pressure-induced bradycardia was associated with increased left ventricular outflow tract obstruction. The carotid sinus pressure-induced increase in the murmur is probably multifactorial: decreased aortic pressure and impedance; increased contractility immediately on sudden slowing of heart rate; further increase in obstruction as the mitral valve systolic anterior movement is enhanced; and delayed vasodilatation maintaining the obstruction even after return of heart rate to precarotid sinus pressure values. An increase in a systolic murmur with carotid sinus pressure is characteristic of HOCM.

As a rule, exercise enhances the rate of discharge of idioventricular rhythms in complete atrioventricular (AV) block. The opposite effect, a sudden drop in the rate of discharge with subsequent resetting of the firing rate, was observed in an 18-year-old boy with chronic complete AV block. Two mechanisms for this paradoxical response to exercise are proposed: (1) delay in discharge of the automatic pacemaker focus by successful penetration of electrotonic potentials from nonconducted P waves across the area of block in the AV conduction system and into the pacemaker focus; and (2) discharge of the pacemaker focus by concealed reentrant extrasystoles. Wedensky inhibition is ruled out because of the resetting of the firing rate.