Pierre Besse

Left ventricular hypertrophy and ventricular dysrhythmic risk in hypertensive patients: evaluation by programmed electrical stimulation.

Left ventricular hypertrophy in hypertensive patients is associated with an increased prevalence of ventricular arrhythmias. Twelve patients with left ventricular hypertrophy assessed by M-mode echocardiography and 12 without left ventricular hypertrophy underwent an electrophysiological study with programmed electrical stimulation. The patients with left ventricular hypertrophy had a prolonged infranodal conduction time which correlated closely with left ventricular mass (r = 0.71; P < 0.001). Programmed electrical stimulation initiated more intraventricular re-entry and unsustained ventricular tachycardia in the group with left ventricular hypertrophy than in the control group, although sustained ventricular tachycardia was never induced. We conclude that ventricular vulnerability is increased in hypertensive patients with left ventricular hypertrophy, especially in those who show electrocardiographic evidence of left ventricular hypertrophy.

Digital-imaging microscopy analysis of calcium release from sarcoplasmic reticulum in single rat cardiac myocytes.

Digital imaging microscopy of fura-2 fluorescence has allowed us to assess the dynamic patterns of local Ca increase in newly isolated rat myocardial cells. Of the myocytes bathed in a saline solution (1.8 mM Ca2+, 37°C, pH 7.4), 10%–20% exhibited local spontaneous contractions. The resting intracellular free calcium concentration ([Ca2+]i) of these cells was 106±4nM versus 77±3 nM for non-contracting cells. The spontaneous contractile activity appeared to be closely related to internal spontaneous Ca waves that spread across the myoplasm (velocity ≈ 50 μm/s, maximal Ca amplitude=195±11nM) along the major axis of the cells. Precise topographical examination of Ca wave propagation indicated a refractory period for internal Ca release. The occurrence of both the generation and propagation of spontaneous Ca increases appeared to be closely dependent on the extent of Ca loading of the cells. Most of our observations were in accordance with the assumption that local Ca overload of the sarcoplasmic reticulum (SR) is the main parameter involved in the spontaneous Ca-release phenomena. Using the same approach, the increase in internal Ca evoked by KCl (50 mM) addition was investigated, and compared with that seen during spontaneous activity. Total [Ca2+]i increase induced by K+ depolarization involved three consecutive local Ca-release patterns: (a) a peripheral Ca enhancement that remained during the total [Ca2+]i increase, (b) subsequent transversal local Ca increases occurring in Z-line regions, (c) longitudinal local Ca increases. In addition, a weak heterogeneous Ca distribution was detected in both peripheral and central parts of resting cardiac cells. Thus, the total Ca increase seemed to result consecutively from a peripheral Ca pool, from junctional SR and from longitudinal structures (possibly longitudinal SR).

Bidirectional Tachycardia. Mechanism Derived from Intracardiac Recordings and Programmed Electrical Stimulation

His bundle recordings and programmed electrical stimulation were performed in a 70‐year‐old woman with bidirectional tachycardia; the recordings demonstrated the infra‐Hissian origin of the tachycardia. Occurrence of the His deflection slightly after the onset of ventricular depolarization suggested that the origin of the tachycardia was located near the His bundle bifurcation. Recording of three atrial sites during tachycardia allowed the study of retrograde atrial activation. Two sets of fairly constant and alternating VA intervals were recorded. This fact is consistent with two ventricular circuits used alternatively. The tachycardia could also be interrupted with a single atrial or ventricular premature beat It is postulated that the tachycardia is due to macroreentry involving the two fascicles of the left branch. This study suggests that reentry may be a possible mechanism in some cases of bidirectional tachycardia. (PACE, Vol. 5, September‐October, 1982)

Diltiazem and left ventricular hypertrophy in renovascular hypertensive rats.

The effects of diltiazem treatment (40-50 mg/kg/day orally for 8 weeks) of left ventricular hypertrophy on systemic and coronary hemodynamics and mechanical cardiac performance were investigated in renovascular hypertensive rats (Goldblatt, two-kidney, one clip). Systemic and coronary hemodynamics were determined by using radioactive microspheres in conscious, unrestrained rats. Mechanical performance was measured on isolated papillary muscle from the same animal. Nine treated hypertensive rats were compared with control groups: 12 untreated hypertensive and nine sham-operated rats. Diltiazem treatment led to an effective but incomplete control of blood pressure (from 208 +/- 5 mm Hg in the untreated hypertensive group to 155 +/- 3 mm Hg in the treated hypertensive group; p less than 0.01) associated with a significant but incomplete decrease of the left ventricular mass (from 3.10 +/- 0.19 mg/g in untreated hypertensive rats to 2.35 +/- 0.04 mg/g in treated hypertensive rats; p less than 0.01). A close correlation was found between left ventricular mass and systolic blood pressure in untreated, treated, and pooled groups (r = 0.84, p less than 0.001, n = 30). The left ventricular weight to systolic blood pressure ratio was equivalent in all three groups, so that the reduction of left ventricular mass in diltiazem-treated rats was commensurate with the reduction of blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Impact of restenosis after optimal directional coronary atherectomy on regional left ventricular function

To assess the effect of optimal directional coronary atherectomy (DCA) on restenosis and left ventricular (LV) function, 95 patients who underwent DCA and adjunctive balloon angioplasty for de novo lesions were prospectively followed for 6 months. Absolute and relative coronary lumen measurements were analyzed with online quantitative coronary angiography. LV volumes, ejection fraction, and segmental wall motion were measured off-line according to the radial method for LV cineangiograms acquired in a right anterior oblique projection. Target vessels were the left anterior descending artery in 63 patients and right coronary artery in 32. Mean (+/- SD) reference diameter was 3.58 +/- 0.65 mm. Mean lumen diameter improved significantly after DCA from 1.19 +/- 0.44 to 3.03 +/- 0.45 mm, yielding a 14 +/- 10% residual stenosis. Overall angiographic restenosis rate (> 50% stenosis in diameter) at control was 23%. In patients without restenosis, there were no significant changes in LV volumes or in LV pressures. In this subgroup, ejection fraction improved significantly in the left anterior descending group (mean difference 3 +/- 10%, p < 0.04). Moreover, there was an increase in fractional shortening of all anterior segments (mean difference 11 +/- 16%, p < 0.005). Improvement in fractional shortening was less marked in the right coronary artery group even without restenosis. We conclude that: (1) optimal DCA can achieve a low restenosis rate in selected large vessels, (2) long-term beneficial effects on regional LV function are possible, particularly in patients with left anterior descending disease and in the absence of coronary restenosis.