Mechanisms and predictors of transient left ventricular dysfunction early after successful percutaneous balloon mitral valvuloplasty.

BACKGROUND: The immediate effects of balloon mitral valvuloplasty (BMV) on left ventricular (LV) function in patients with mitral stenosis are still controversial. The aim of this study was to investigate the mechanisms and potential clinical, echocardiographic and hemodynamic predictors of transient LV dysfunction occurring in patients with mitral stenosis early after successful percutaneous BMV. METHODS: Sixty patients without residual mitral regurgitation were divided into two groups according to the changes in the left atrial (LA) pressure 15 min after successful BMV: 18 patients (group A) did not present with any reduction in LA pressure, and underwent nitroglycerin administration (0.4 mg, sublingually). The remaining 42 patients (group B) presented with a decrease in LA pressure. RESULTS: At baseline, both the mitral valve gradient and area assessed at echocardiography and during cardiac catheterization were similar in groups A and B. Group A patients presented with, however, higher LV early- and end-diastolic pressures and peak V waves during cardiac catheterization both prior to and 15 min after BMV than group B patients (all p values < 0.05). In group A, nitroglycerin administration was associated with a decrease in LV end-diastolic pressure (p = 0.049), LA pressure (p < 0.001), and peak V wave (p < 0.001) that was still persistent 30 min after its administration, reaching values similar to those observed in group B early after BMV. At multivariate analysis, the only independent predictors of LV dysfunction early after BMV were found to be LV early- (p = 0.015) and end-diastolic (p = 0.023) pressures at baseline and the Wilkins' score (p = 0.004). CONCLUSIONS: After successful BMV a transient lack of LV adaptation to the increased LV preload resulting in a persistently elevated LA pressure is predicted by higher baseline LV diastolic filling pressures and higher Wilkins' scores. It is promptly and steadily reversed by nitroglycerin administration through a transient LV unloading, thus allowing a correct hemodynamic evaluation of the immediate results of the procedure.

Left ventricular decompression through a patent foramen ovale in a patient with hypertrophic cardiomyopathy: a case report.

The foramen ovale is considered an unidirectional flap-like valvular structure. Yet, it may increase in size and allow a continuous left-to-right shunt in order to reduce left ventricular filling pressures. We report the case of a 63-year-old woman with hypertrophic cardiomyopathy, referred for percutaneous closure of a coexisting secundum atrial septal defect. Before catheterization, however, transesophageal echocardiography revealed a continuous left-to-right shunt within the atrial septum, thus suggesting the diagnosis of patent foramen ovale with stable left-to-right shunt. At catheterization, performed under general anesthesia and transesophageal echocardiographic monitoring, left ventricular early- and end-diastolic pressures were 2 and 12 mmHg and pulmonary-to-systemic flow ratio was 1.4. Provocative maneuvers were not able to reverse the shunt. In order to assess the effect of the increased left ventricular preload due to the abolition of the shunt, an Amplatzer sizing balloon was inflated for 5 minutes across the patent foramen ovale. Diastolic pressures rose up to 5 and 18 mmHg, respectively. Such a worsening of left ventricular function suggested us not to perform the closure procedure. Transcatheter closure of any interatrial communication with stable left-to-right shunt induces an abrupt overload of the left ventricle that may cause acute heart failure in patients with coexisting left ventricular dysfunction. The hemodynamic evaluation of left ventricular function during transient abolition of the shunt is an useful tool in order to establish the most correct therapeutic strategy. The closure procedure should not be performed if a worsening of left ventricular function occurs.

Chest pain after coronary artery stent implantation.

A sizeable proportion of patients who undergo successful coronary artery stent implantation experiences chest pain immediately after the procedure and/or in the following months in the absence of in-stent restenosis. We investigated this phenomenon in 57 consecutive patients with stable angina who underwent successful stent implantation. Chest pain characteristics were assessed before stent implantation and during 6-month follow-up. All patients underwent coronary angiography within 6 months of the procedure 48 hours after exercise thallium-201 perfusion scintigraphy. Patients who did not exhibit in-stent restenosis underwent an ergonovine test at the end of routine coronary angiography. During follow-up, 15 patients complained of chest pain. Six of these patients exhibited scintigraphic evidence of myocardial ischemia and in-stent restenosis at angiography. In the remaining 9 patients, chest pain occurred in the absence of in-stent restenosis at angiography. In 8 of these patients intracoronary ergonovine administration reproduced their habitual pain, whereas it did not cause any pain in the 42 patients who were completely asymptomatic at follow-up and without in-stent restenosis. Ergonovine caused more intense vasoconstriction and nitroglycerin caused more intense vasodilation of the reference coronary diameter in patients with than in patients without ergonovine-induced pain (-17 +/- 3 vs -9 +/- 3%, p <0.001; 9 +/- 6 vs 5 +/- 4%, p <0.02, respectively). In conclusion, chest pain with features similar to habitual angina occurs in the absence of in-stent restenosis in 1/5 of patients after stent implantation and appears to be associated with more intense coronary vasoreactivity.

Analgesic effect of bamiphylline on pain induced by intradermal injection of adenosine.

Adenosine is known to cause pain when injected intravenously or intra-arterially. We have conducted a double-blind placebo-controlled study by injecting adenosine intradermally in 6 healthy subjects (5 male, 1 female; age: 27-34 years). Pain was assessed using the visual analogue scale. The intradermal injection of 2 mumol of adenosine produced pain significantly greater than normal saline after 15 sec (T0) (29 +/- 13 vs. 7 +/- 6 mm, P = 0.004), 1 min after T0 (13 +/- 9 vs. 0 +/- 0 mm, P = 0.002) and 2 min after T0 (4.5 +/- 5 vs. 0 +/- 0 mm, P < 0.05). There was evidence of hyperalgesia to mechanical and heat stimuli at the injection site (primary hyperalgesia). There was no evidence of mechanical hyperalgesia in the cutaneous area surrounding the injected site (secondary hyperalgesia). In all cases the intradermal injection of adenosine produced local hyperemia (mean surface are: 147 +/- 69 mm2) which was absent after placebo injection. The pre-injection of bamiphylline, a rather selective antagonist of A1 adenosine receptors, differently from placebo, completely suppressed the adenosine-induced pain after 15 sec (T0) (15 +/- 10 vs. 0 +/- 0 mm, P = 0.002) and 1 min after T0 (9 +/- 7 vs. 0 +/- 0 mm, P = 0.002). No anesthesia to heat, cold and mechanical stimuli was detected at the bamiphylline site. The adenosine-induced erythematous area was wider at the bamiphylline pre-injected site than at the placebo pre-injected site (173 +/- 114 vs. 119 +/- 85 mm2).(ABSTRACT TRUNCATED AT 250 WORDS)