Francesco Cucchini

The metabolical effects of l-carnitine in angina pectoris☆

We determined the effects of L-carnitine on myocardial metabolism in 18 patients with angiographically-proven coronary artery disease, subjected to two rapid coronary sinus pacing evaluations. L-Carnitine converted lactate production to extraction and increased the percentage of free fatty acid extraction. These results suggest that L-carnitine may be of use to improve the metabolism of coronary artery disease patients.

Aortic Intramural Hematoma: An Increasingly Recognized Aortic Disease

Aortic intramural hematoma (IMH) is a rarely diagnosed pathological condition that is not well characterized to date. We diagnosed IMH in 4 of 31 patients with suspected aortic dissection admitted to our coronary care unit from 1992 to 1995. In all 4 cases, IMH was located in the ascending aorta. At the time of hospitalization, all patients showed tachycardia, hypotension and pericardial effusion. Diagnosis of IMH was made by transesophageal echocardiography and computed tomography. We performed aortography in 2 patients, but it was non-diagnostic in both of them. One patient died before surgery. Autopsy confirmed the diagnosis of IMH and showed severe pericardial effusion. In another patient, the diagnosis was confirmed during successful surgery, while the remaining 2 patients recovered after medical therapy. The 3 surviving patients are still under follow-up control 12, 16 and 20 months after the initial acute event. We briefly discuss the epidemiological, clinical, diagnostic, therapeutic and prognostic aspects of IMH.

Comparison of Five Different Stress Testing Methods in the ECG Diagnosis of Coronary Artery Disease

Five different stress testing methods: bicycle ergometer exercise (BE), treadmill exercise (TD), isoproterenol infusion test (IPN), dopamine infusion test (DPM), and atrial pacing (AP), were performed on 90 male patients who underwent coronary arteriography. Ischemic S-T segment depression of 1.0 mm or greater was used as the criterion for a positive test. Within the group of 56 subjects having significant coronary artery disease (CAD) the diagnostic sensitivity of the single tests was as follows: 64.3% for BE, 66.1% for TD, 69.6% for IPN, 41.1% for DPM, 75.0% for AP. For the 34 subjects with no CAD the folowing specificity was found: 88.2% for BE and for TD, 82.3% for IPN, 85.3% for DPM, 63.8% for AP. When the results of the different tests were combined, it was seen that the association of an ergometric test with IPN enhanced the sensitivity of the exercise test (p less than 0.05) without significantly decreasing the specificity.

Effects of verapamil and nifedipine on rate of left ventricular relaxation in coronary arterial disease patients

We have evaluated the effects of nifedipine and verapamil on rate of left ventricular relaxation in 26 patients having coronary arterial disease with normal ejection fraction and normal left ventricular contractility. None of the patients had myocardial infarction. All patients showed normal contractile indices and abnormally high values of T constant, neg, dP/dt and left ventricular protodiastolic pressure, suggesting an impairment of left ventricular relaxation. Nifedipine, injected intravenously (15 micrograms/kg) in 14 patients induced a significant reduction of afterload parameters and an increase of contractility. Nifedipine also improved left ventricular relaxation, as it induced a reduction of the T constant from 42 +/- 2 msec to 33 +/- 2 msec (P less than 0.01). It induced a tendency to a reduction of negative dP/dt and protodiastolic pressure without reaching statistical significance. Verapamil, injected intravenously in the remaining 12 patients (0.1 mg/kg as a bolus followed by chronic infusion of 0.005 mg/kg/min for 3 min) induced a reduction of the T constant from 43 +/- 10 to 37 +/- 6 msec (P less than 0.01). It reduced the negativity of dP/dt from 2302 +/- 273 to 2021 +/- 252 mm Hg/sec (P less than 0.05) and of left ventricular protodiastolic pressure from 3.2 +/- 1.4 to 1.5 +/- 1.1 mm Hg (P less than 0.01). Verapamil, like nifedipine, reduced the afterload parameters although to a lesser extent. It did not substantially affect the left ventricular contractility. These data suggest that abnormalities of left ventricular relaxation may precede changes in systolic function and that nifedipine and verapamil favourably modify the indices of left ventricular diastolic function in patients with coronary arterial disease.

Left atrial appendage systolic forward flow

T he advent of transesophageal echocardiography (TEE) has greatly improved the ability to detect cardiac sources of embolism. 1 This technique allows an easy and accurate evaluation of anatomic structure and function of the left atria1 appendage (LAA).2-4 Although it is well established that there is an association of LAA thrombi and left atria1 spontaneous echo contrast with a history of peripheral embolism,2 only recently has a study focused on LAA Doppler flow signals.3 Kortz et al3 reported a quadriphasic pattern of LAA flow in normal subjects without overlapptig of tachycardia-related waves: a diastolic forward flow just after mitral valve opening is followed by a diastolic backward flow due to LAA recoil; subsequently, a forward and a backward flow wave respectivCly due to LAA contraction and relaxation can be detected. . . . We report our observations on a new LAA flow pattern characterized by the presence of an additional systolic forward flow wave after LAA relaxation. After the first occasional observation of a systolic LAA flow wave, a study was undertaken to characterize this new tiding. TEE was prospectively performed in 62 consecutive patients with sinus rhythm. Reasons for the examinations were determination of source of embolism (62%), assessment of suspected endocarditis (lo%), detection of aortic and mitral valve disease (18%), and evaluation of valve prosthesis (10%). Ten patients were excluded from the sttidy because of inadequate representation of the LAA. The study group consisted of 12 patients (mean age 51 f 16 years) in whom the presence of LAA systolic forward flow was observed. Anesthesia of the hypopharynx was p&formed with 10% lidocaine spray. For sedation, patients were given a mean intravenous dose of 2 mg of midazolam. TEE was performed using a Sonos 1500 (Hewlett-Packard, Andover, Massachusetts), a Sonolayer SSH 140-A (Toshiba, Tokyo, Japan), or a Domier (Deutsche Aerospace, Munich, Germany) ultrasound system equipped with 5 MHz multiplane phased-array transducers. The LAA was mainly visualized in the longitudinal view and the probe adjusted to maximize its dimensions. Flow velocities were obtained by positioning the sample volume inside the left atria1 appendage at the point that offered the best alignment with its flow and avoided the noise signal due to wall motion. Furthermore, color Mand B-mode of the left atrial appendage flow were recorded. The presence of systolic forward flow after LAA relaxation was assumed when there were concomitant pulsed Doppler signal and color Band M-mode findings. Pulmonary venous velocity recordings were obtained with

Effects of acute k-strophantidin administration on left ventricular relaxation and filling phase in coronary artery disease

In 10 patients with coronary artery disease, preserved left ventricular (LV) performance and absence of previous myocardial infarction, the effects of an acute intravenous administration of k-strophantidin (0.005 mg/kg over 10 minutes) on selected parameters of both LV systolic and diastolic function, including relaxation, were evaluated. An increase in positive first derivative of LV pressure (dP/dt) and in the ratio between dP/dt and the pressure developed (dP/dt/P) (1,530 +/- 287) 1,600 +/- 329 mm Hg/s [p less than 0.05], and 30 +/- 6 to 34 +/- 8 s-1 [p less than 0.05], respectively) demonstrated the inotropic effect of k-strophantidin, whereas volumetric parameters of systolic function (end-systolic and stroke volume indexes, and ejection fraction) did not show any significant change. However, LV relaxation was impaired by k-strophantidin injection; in fact, mean values of T constant were significantly increased from 50 +/- 12 to 55 +/- 13 ms (p less than 0.01). Lowest LV and end-diastolic pressures increased from 8 +/- 4 to 11 +/- 4 mm Hg (p less than 0.05) and from 17 +/- 6 to 20 +/- 8 mm Hg (p less than 0.05), respectively. The end-diastolic volume and maximal rate of volumetric increase during the early and late filling phases were not modified by k-strophantidin. Mean aortic pressure increased from 110 +/- 10 to 120 +/- 12 mm Hg (p less than 0.001). Therefore, in patients with coronary artery disease and LV preserved performance, an acute intravenous administration of k-strophantidin appears to stimulate contractility and to worsen relaxation, and minimal LV and end-diastolic pressures.

Effect of dobutamine on left ventricular relaxation and filling phase in patients with ischemic heart disease and preserved systolic function

SummaryThe beneficial effects of dobutamine on left ventricular systolic and diastolic phases have been described in patients with congestive heart failure. Its influence on left ventricular diastolic phase in patients with preserved systolic function, absence of dys- or akinetic areas, and left ventricular dilatation has not yet been adequately investigated. Thus a simultaneous echo-Doppler and hemodynamic study was performed in 15 patients with ischemic heart disease and preserved systolic function in order to assess the effect of dobutamine on left ventricular relaxation and filling phase. The infusion of dobutamine at a rate of 10 µg/kg/min induced a marked inotropic action, as shown by the significant increase in positive dP/dt (from 1392±224 to 2192±295 mmHg/sec, p<0.001), dP/dt/P (from 32±8.1 to 50±17 sec−1; p<0.0001), and in peak of systolic pressure (from 143±25 to 168±36 mmHg; p<0.005). In addition, dobutamine reduced the end-systolic volume index (from 30±16 to 26±19 ml/m2; p<0.05), the end-systolic stress (from 222.2±65.3 to 198.4±84 g/cm2; p<0.006), and had favorable effects on relaxation and the early filling phase. The constant T (tau) significantly decreased (from 46±9 to 36±11 msec; p<0.0001), while the left atrial left ventricular lowest pressure difference from 7.2±3.3 to 13.3±4.7 mmHg; p<0.05), peak E velocity (from 0.52±0.08 to 0.65±0.18 m/sec; p<0.05), and E velocity integral (from 12±3.2 to 15.39±6.10 cm; p<0.05) significantly increased. In contrast, the late diastolic filling did not change. The positive effect of dobutamine on the diastolic phase might be explained by its mechanism at the subcellular level and by the reduction of both left ventricular end-systolic volume and end-systolic stress. We might conclude that in coronary artery disease patients with preserved systolic function dobutamine improves both relaxation and the early filling phase; these results add further information to the pharmacological effects of this drug.

Threshold energy dose for enzyme release after direct-current countershock

Serial measurement of serum total creatine kinase and creatine kinase MB isoenzyme was prospectively performed by photometric assay in 82 consecutive patients (55 male and 27 female; mean age 62 +/- 11 years) after elective DC countershock for atrial flutter or fibrillation. Enzyme release is commonly observed to follow DC shock; the related energy threshold for enzyme release, however, a parameter with potential clinical usefulness, has not yet been determined. The energy dose was individually titrated but the anterolateral paddle-electrode location was used in all cases. The mean +/- S.D. (range) of shock number, peak energy level and cumulative energy dose normalized to body weight were respectively: 1.7 +/- 0.9 (1-5), 228.6 +/- 87.6 (75-400) J and 5.26 +/- 3.74 (1.0-19.7) J/kg. All these parameters had highly significant positive correlation with enzyme release (P < 0.0001), which peaked 16 h after countershock. Only creatine kinase levels changed significantly vs. baseline (P < 0.0001). As evidenced by dose vs. effect scattergram, the energy threshold value for enzyme release was around 4 J/kg for creatine kinase and 6 J/kg for creatine kinase MB isoenzyme. These energy dose figures may provide clinical usefulness to avoid unnecessary muscle damage; moreover, they may be used as a reference when enzyme elevations interfere with the diagnosis of a concomitant ischemic acute myocardial infarction.

Different effects of acute intravenous administration of k-strophantidin and prenalterol on the diastolic phase of left ventricular function in patients with coronary arterial disease

In 21 patients with coronary arterial disease, and with maintained (or mildly depressed) systolic function, we studied the effects of two well-known inotropic agents, namely prenalterol and k-strophanthidin, on the diastolic phase. Selected variables of both systolic and diastolic function were assessed at controlled heart rate by cardiac catheterization and left ventriculography before and after acute intravenous administration of the beta 1 agonist prenalterol (35 micrograms/kg for 3 min) and of k-strophanthidin (0.008 mg/kg for 5-10 min). Ten patients received prenalterol, and 11 patients were injected with k-strophanthidin. Administration of prenalterol induced a remarkable diminution of end-systolic volume index (mean values from 41.8 +/- 11.9 to 32.2 +/- 10.4), while k-strophanthidin showed only a tendency towards a decrease (mean values from 43.4 +/- 13.2 to 40.7 +/- 15.1). After k-strophanthidin, we did not observe any significant changes in the peaks of maximal rate in volumetric increase during filling phase whereas, after prenalterol, a noteworthy increase of the first peak was accompanied by a significant decrease of the second peak. The lowest and end filling left ventricular pressures were decreased by prenalterol (mean values from -0.8 +/- 0.1 to -2 +/- 0.5 and from 10.6 +/- 4.6 to 4.1 +/- 1.1 respectively), whereas k-strophanthidin increased left ventricular end diastolic pressure (mean values from 11.6 +/- 4.3 to 17.1 +/- 9.1). Prenalterol induced a relevant increase of ejection fraction (mean values from 0.52 +/- 0.1 to 0.61 +/- 0.008), whereas k-strophanthidin produced only a nearly significant (P less than 0.06) mild increase (mean values from 0.51 +/- 0.06 to 0.54 +/- 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)

Left Innominate Vein Aneurysm Finding during Pacemaker Lead Insertion

Thoracic vein aneurysms are very rare vascular lesions, usually detected as incidental findings. We describe the case of a patient with an advanced atrioventricular block who underwent definitive pacemaker implantation. In order to explain the difficult advancement of a pacemaker lead, vein angiography was performed during the procedure and a large innominate vein aneurysm was observed. Successful lead placement was then performed without further complications.