Usefulness of dipyridamole transesophageal echocardiography in the evaluation of myocardial ischemia and coronary artery flow.

High-dose dipyridamole transesophageal stress echocardiography has recently been proposed as a useful and safe method to assess myocardial ischemia in patients with poor transthoracic acoustic window. It has also been shown that transesophageal echocardiography (TEE) allows the study of coronary blood flow reserve (CBFR) in the left anterior descending artery (LAD). The aim of our study was to assess whether the morphologic information and pathophysiologic data on CBFR and myocardial ischemia can be collected by a single stress TEE without comprimizing its feasibility, safety and accuracy. We studied, 29 patient with known or suspected CAD (previous myocardial infarction or angina) (Group A), and as a control group, we studied 11 patients with mitral disease or mitral prostheses (Group B). All patients underwent the coronary angiography. None of Group B patients showed significant coronary artery stenosis (> 70%). In baseline conditions left ventricular wall motion and LAD coronary blood flow velocity (CBFV) were also evaluated. The following CBFV parameters were measured: maximal diastolic velocity (MaxDV), mean diastolic velocity (MnDV), maximal systolic velocity (MaxSV), mean systolic velocity (MnSV). The ratios of dipyridamole to rest maximal and o mean to diastolic velocities (MaxDV-Dip/Max DV-rest; MnDv-Dip/MnDV-rest) were measured as indexes of CBFR. No side effects were observed and the test could be completed in all patients (feasibility 100%). Wall motion analysis was adequate in all patients (feasibility 100%). Comparison between wall motion analysis was obtained and angiographic findings shown that the overall sensitivity and specificity of TEE were 84% and 93% respectively. Sensitivity for one, two and three vessel disease was 60%, 70% and 100%, respectively. LAD CBFV was adequately recorded in 85% of patients. CBFR parameters showed a significant difference between the two groups (Max DV-Dip/Max DV-rest: 1.67 +/- 0.7 vs. 2.73 +/- 0.6, P < 0.001); comparison between Group B patients and those of Group A with angiographically documented LAD stenosis showed a statistically significant difference in CBFR parameters (MaxDV-Dip/MnDV-rest, 2.73 +/- 0.6 vs. 1.65 +/- 0.7, P < 0.001, MnDV-Dip/MnDV-rest, 2.56 +/- 0.5 vs. 1.69 +/- 0.6 < 0.001). We conclude that transesophageal stress echocardiography is a useful method to study CAD and that it is possible to assess both morphologic and pathophysiologic information during a single examination.

Effects of oral propafenone therapy on chronic myocardial pacing threshold.

The effects of oral propafenone therapy on pacing threshold were studied in 36 patients chronically paced for sick sinus syndrome or AV block. The pacemakers, all unipolar models and with noninvasive threshold measurement facilities, were: 9 VVI, 15 AAI, and 12 DDD. Each patient received an initial propafenone dose of 450 mg/day, that in 18 cases was increased to 900 mg/day. Threshold was tested at baseline and at each dosage after 7 days of therapy. With the lower propafenone dosage the threshold, measured at 2.5 V, rose from 0.14 +/- 0.10 to 0.21 +/- 0.16 msec (+55%) in the atrium (P less than 0.0001) and from 0.10 +/- 0.08 to 0.15 +/- 0.09 msec (+63%) in the ventricle (P less than 0.0001). In the 18 patients who received both dosages, the mean atrial and ventricular threshold increased from 0.12 +/- 0.10 to 0.17 +/- 0.14 msec with the lower dose and to 0.27 +/- 0.22 msec (+125%) with the higher dose (P less than 0.0001 for both increments). With the 900 mg/day dose, a threshold increment greater than or equal to 300% was observed in 15% of the stimulated chambers. A good linear correlation (r = 0.76) was found between the ventricular threshold increment and the drug induced QRS widening. In conclusion, treatment with oral propafenone increases atrial and ventricular stimulation threshold in pacemaker patients. Threshold increment is dose dependent and proportional to the drug induced QRS widening. In the majority of the cases the threshold increment is not clinically significant, but caution must be used in prescribing high doses of the drug to patients with high baseline threshold.

[Malignant ventricular hyperkinetic arrhythmia: role of permanent electric treatment]. / Aritmie ipercinetiche ventricolari maligne: ruolo del trattamento elettrico definitivo.

While the technics of cardiac pacing have shown to have a precise role in the diagnosis and treatment of ventricular arrhythmias on a temporary basis, the role of permanent antiarrhythmic devices (PAD) in the treatment of these arrhythmias is still ill defined mainly because of the technological limits concerning the pacemakers and the frequent complications observed during the attempts to interrupt such tachycardias. On the basis of the available data and of theoretical considerations, three groups of pts susceptible of treatment with PAD can be selected: a) pts with brady-dependent arrhythmias where PAD is used as a prophylactic mean; b) pts with recurrent sustained ventricular tachycardia refractory to medical treatment, in whom PAD can be used to interrupt tachycardia; c) pts affected by ventricular fibrillation or rapidly deteriorating ventricular tachycardia (sudden death pts), refractory to conventional treatment, in whom the implantable defibrillator represents the only therapeutic possibility. Even if scanty, the data available seem to confirm that PAD does have a role in the treatment of malignant arrhythmias, although in selected cases and almost always together with drug treatment.

Rhythm characteristics of plasma renin, aldosterone and cortisol in five subtypes of mesor-hypertension.

The possible role of the renin-angiotensin system and ACTH in controlling the temporal organization of circadian rhythm of aldosterone was studied in patients with mesor-hypertension (MH) by simultaneous radioimmunological determinations of within-day changes in plasma renin, aldosterone and cortisol. Thirty-nine uncomplicated, untreated mesor-hypertensive patients, divided in subtypes, were examined. The interrelationship between the rhythm components revealed that the circadian cyclicity of aldosterone in both mesor-normotensive and mesor-hypertensive subjects, with either normal or high renin patterns, has a similar timing in acrophase with renin periodicity, which leads the circadian cortisol rhythm. In low-renin mesorhypertensive subjects a circadian rhythm of aldosterone and cortisol, but not of renin, remains demonstrable. The confidence limits of the estimated acrophase for circadian cortisol rhythm do not, however, overlap the confidence arcs of the aldosterone phase. These findings suggest that in normal or high renin MH subjects the aldosterone rhythmicity is mainly controlled by the renin-angiotensin system. Conversely in low-renin MH subjects the temporal organization of the aldosterone circadian sequences seems to be completely independent of renin-angiotensin control.

Renal-portal shunt to restore normal reninism and blood pressure in experimental renovascular hypertension in dogs.

The role of the liver in the metabolism of renin was evaluated in dogs with high plasma renin and hypertension due to experimental bilateral renal artery stenosis. Ten adult dogs were studied in three consecutive phases: (1) basal conditions, (2) with bilateral ischemic kidneys, and (3) after derivation of renal vein blood into the portal system. Secretion, total clearance, hepatic clearance, and hapatic extraction of renin were estimated in each phase by measuring plasma renin activity (PRA) in blood collected simultaneously from arteries, inferior vena cava, vena porta, hepatic and renal veins, and by determining renal and hepatic blood flow. Blood pressure was measured by intra-arterial catheterization. The results demonstrated an increase in the hepatic metabolism of renin when the hyper-reninemic patterns of renal blood directly perfused the liver. Under these conditions, hepatic and circulating renin fell to basal values and blood pressure returned to normal.

Beta-adrenergic regulation of circadian rhythmicity of the renin-angiotensin-aldosterone system in five subtypes of essential hypertension.

The possible implication of the beta-sympathoadrenergic system in regulating the rhythmicity of the renin-angiotensin-aldosterone system (RAAS) was studied in ten normotensive volunteers and in thirty-nine essential hypertensive patients. The study was carried out by simultaneous radioimmunological measurements of diurnal levels of plasma renin and aldosterone before and during acute oral medication of beta-adrenoceptors with propranolol. Acute beta-blockade was seen to blunt the circadian periodicity of plasma renin and aldosterone in normotensives and in hypertensives with normal or high renin patterns. Conversely propranolol was seen to be ineffective in low-renin patients. The disappearance of the circadian rhythms under beta-adrenoceptor blockade tends to suggest the existence of a beta-adrenergic control of RAAS cyclicity in normal condition, as well as in normal or high renin essential hypertension. The inefficacy of propranolol in hyporeninemic hypertensives is consistent with the hypothesis that low-renin essemtoa; juertemsopm os a state in which the sympatho beta-adrenergic mechanism controlling the function of RAAS has no biologic time structure.