[Hypothenar hammer syndrome; rare arterial disorder of the hand due to blunt trauma]. / Hypothenar-hamersyndroom: zeldzame arteriële stoornis van de hand door stomp trauma.

The hypothenar hammer syndrome is a condition characterised by ischaemia of a finger secondary to thrombosis or an aneurysm or pseudoaneurysm of the ulnar artery in the hand. It typically occurs in the dominant hand of middle-aged men whose occupational or recreational activities require the use of the hand as a hammer. Arteriography is considered to be the gold standard for diagnosing this condition. Severe symptomatic cases are treated by surgical resection and revascularisation. The pathophysiology of this syndrome, its diagnosis and its management are discussed in this article by means of two representative cases, each having a different clinical presentation, diagnostic method and treatment.

Should amiodarone or lidocaine be given to patients who arrest after cardiac surgery and fail to cardiovert from ventricular fibrillation?

A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was whether the administration of amiodarone or lidocaine in patients with refractory VT/VF after cardiac surgery results in successful cardioversion. Altogether more than 434 papers were found using the reported search, from which 23 articles were used to answer the clinical question. No randomized trials have been found in which amiodarone was studied in patients with refractory VF/VT after cardiac surgery. Recommendations on the use of amiodarone in patients with refractory VF/VT in both European and American 2005 Guidelines on Resuscitation are mainly based on expert consensus and are supported by a few randomized trials in patients with out-of-hospital cardiac arrest. We would therefore recommend that amiodarone is the first line drug that should be used in patients with refractory ventricular arrhythmias after cardiac surgery that persist after three failed attempts at cardioversion. Lidocaine should only be used if amiodarone is not available or if its use is contraindicated. Amiodarone should be administered as an intravenous bolus of 300 mg after the third unsuccessful shock.

Chronic right ventricular pressure overload results in a hyperplastic rather than a hypertrophic myocardial response.

Myocardial hyperplasia is generally considered to occur only during fetal development. However, recent evidence suggests that this type of response may also be triggered by cardiac overload after birth. In congenital heart disease, loading conditions are frequently abnormal, thereby affecting ventricular function. We hypothesized that chronic right ventricular pressure overload imposed on neonatal hearts initiates a hyperplastic response in the right ventricular myocardium. To test this, young lambs (aged 2-3 weeks) underwent adjustable pulmonary artery banding to obtain peak right ventricular pressures equal to left ventricular pressures for 8 weeks. Transmural cardiac tissue samples from the right and left ventricles of five banded and five age-matched control animals were studied. We found that chronic right ventricular pressure overload resulted in a twofold increase in right-to-left ventricle wall thickness ratio. Morphometric right ventricular myocardial tissue analysis revealed no changes in tissue composition between the two groups; nor were right ventricular myocyte dimensions, relative number of binucleated myocytes, or myocardial DNA concentration significantly different from control values. In chronic pressure overloaded right ventricular myocardium, significantly (P < 0.01) more myocyte nuclei were positive for the proliferation marker proliferating cellular nuclear antigen than in control right ventricular myocardium. Chronic right ventricular pressure overload applied in neonatal sheep hearts results in a significant increase in right ventricular free wall thickness which is primarily the result of a hyperplastic myocardial response.

Effects of acute left ventricular unloading on right ventricular function in normal and chronic right ventricular pressure-overloaded lambs.

OBJECTIVE: Right ventricular pressure overload occurs in several types of (congenital) heart disease, as well as in pulmonary disease. Clinical outcome in some of these patient groups might in part be related to left ventricular loading conditions. The effects of left ventricular unloading on the function of the hypertrophic right ventricle have not been studied. We aimed to study the effects of left ventricular unloading on right ventricular hemodynamics and contractility in an animal model of chronic right ventricular pressure overload. METHODS: In lambs the pulmonary artery was chronically banded to increase right ventricular pressure to systemic levels. After 8 weeks, right ventricular contractility and hemodynamic function were assessed in these lambs, as well as in age-matched control animals, by using a combined pressure-conductance catheter in the right ventricle during baseline conditions and during complete bypass of the left ventricle. RESULTS: In both groups acute left ventricular unloading significantly decreased left ventricular pressure to low levels while aortic pressure was maintained. In the right ventricle of the control group, both end-systolic and end-diastolic volumes increased with left ventricular unloading (P <.01) while end-systolic pressure was maintained. Cardiac output was unchanged despite decreased right ventricular contractility. In the banding group acute left ventricular unloading also decreased right ventricular contractility but increased cardiac output. During acute left ventricular unloading, diastolic stiffness was unchanged in the control group, whereas it was significantly decreased in the banding group. CONCLUSIONS: Both in normal hearts and in hearts subject to chronic right ventricular pressure overload, acute left ventricular unloading decreases right ventricular contractility. Although no effects on cardiac output are encountered in normal hearts during left ventricular bypass, cardiac output is improved in right ventricular pressure-overloaded hearts, most likely related to improved right ventricular diastolic compliance.

Chronic and adjustable pulmonary artery banding.

OBJECTIVE: Banding of the pulmonary artery might be required to prevent pulmonary vascular damage in patients with increased pulmonary artery flow and to retrain the left ventricle in preparation for an arterial switch operation in patients with congenitally corrected transposition of the great arteries. Readjustment of the pulmonary artery band might be required in the postoperative period. In this study we aimed to test the feasibility of a novel device for bidirectionally adjustable pulmonary artery constriction. METHODS: A hydraulic main pulmonary artery occluder was implanted in lambs and gradually inflated to create right ventricular pressure overload at a systemic (aortic) level. During the following period (up to 12 weeks), this pressure overload was monitored by measuring aortic and right ventricular pressures by means of implanted subcutaneous reservoirs. If required to maintain the right ventricular pressure overload at a systemic level in the growing animals, the occluder was deflated through a third subcutaneous reservoir. RESULTS: After the banding period (average of 64 +/- 8 days), the main pulmonary artery cuff could still be adjusted, and the animals showed no clinical signs of heart failure. Histologic analysis of the pulmonary artery showed extensive fibrosis, a giant cell response around the device, and small areas of tissue necrosis; complete transmural necrosis was not detected. CONCLUSIONS: This device allows adjustment of the pulmonary artery cuff in a precise manner over a prolonged period of time without surgical reintervention. Potentially, the device might have applications for clinical use in children with congenital heart disease.

Indexes of diastolic RV function: load dependence and changes after chronic RV pressure overload in lambs.

Diastolic function is a major determinant of ventricular performance, especially when loading conditions are altered. We evaluated biventricular diastolic function in lambs and studied possible load dependence of diastolic parameters [minimum first derivative of pressure vs. time (dP/dt(min)) and time constant of isovolumic relaxation (tau)] in normal (n = 5) and chronic right ventricular (RV) pressure-overloaded (n = 5) hearts by using an adjustable band on the pulmonary artery (PAB). Pressure-volume relations were measured during preload reduction to obtain the end-diastolic pressure-volume relationship (EDPVR). In normal lambs, absolute dP/dt(min) and tau were lower in the RV than in the left ventricle whereas the chamber stiffness constant (b) was roughly the same. After PAB, RV tau and dP/dt(min) were significantly higher compared with control. The RV EDPVR indicated impaired diastolic function. During acute pressure reduction, both dP/dt(min) and tau showed a relationship with end-systolic pressure. These relationships could explain the increased dP/dt(min) but not the increased tau-value after banding. Therefore, the increased tau after banding reflects intrinsic myocardial changes. We conclude that after chronic RV pressure overload, RV early relaxation is prolonged and diastolic stiffness is increased, both indicative of impaired diastolic function.