A review of rhythm disorders in cardiac hypertrophy

Ventricular arrhythmias frequently occur in both experimental and human left ventricular hypertrophy. The mechanism of arrhythmia is not clear but appears to be related to the process of hypertrophy and the accompanying fibrosis rather than to coexistent coronary artery disease or diuretic-induced hypokalemia. Although neither the independent prognostic value of ventricular arrhythmias nor the benefit of antiarrhythmic therapy has been demonstrated in prospective studies involving hypertensive patients, it is possible that appropriate antiarrhythmic therapy may reduce mortality in selected patients with severe hypertrophy.     

Hypertensive left ventricular hypertrophy risk: beyond adaptive cardiomyocytic hypertrophy

The heart is a remarkably adaptive organ, capable of increasing its minute output and overcoming short-term or prolonged pressure overload. The structural response, in addition to the foregoing functional demands, is that of myocardial hypertrophy. Then, why should an adaptive response increase cardiovascular risk in hypertensive patients with left ventricular hypertrophy (LVH)? Evidence shows that the functional performance of hypertrophied cardiomyocytes is impaired, and that additional alterations develop in cardiomyocytes themselves, the extracellular matrix and the intramyocardial vasculature, leading to myocardial remodelling and providing the basis for the adverse prognosis associated with pathological LVH in hypertensive patients (i.e., hypertensive heart disease, HHD). As molecular information accumulates, the pathophysiological understanding and the clinical approach to HHD are changing. The time has come to develop novel diagnostic and therapeutic strategies aimed at improving the prognosis of HHD on the basis of reversing or even preventing the aforementioned changes in the ventricular myocardium.     

Arterial hypertension, myocardial hypertrophy and disorders of cardiac rhythm induced by ligation of the left coronary artery in the rat

Cardiac hypertrophy and hypertension are major elements in sudden cardiac death in patients with coronary artery disease. To investigate in animals the hypothesis that left ventricular hypertrophy (LVH) and/or hypertension increase the incidence of severe ventricular arrhythmias, we have undertaken a 30 min period of coronary artery ligation in anaesthetized spontaneously hypertensive rats (SHR), normotensive (NT) Wistar Kyoto (WKY) and Wistar (W) rats. Mean systolic blood pressure (SBP) was 190 +/- 4 mmHg in SHR vs 123 +/- 5 mmHg in WKY and 116 +/- 4 mmHg in W (p less than 0.001). LVH index was 2.81 +/- 0.04 in SHR vs 196 +/- 0.03 in WKY and 1.65 +/- 0.05 in W (p less than 0.01). Incidence (IVF) and duration (DVF) of ventricular fibrillation were significantly more elevated in SHR than in NT rats. IVF was 100 p. 100 in SHR vs 36 p. 100 in WKY and 27 p. 100 in W (p less than 0.001); DVF was 61 +/- 17 s in SHR vs 6 +/- 6 s in WKY and W (p less than 0.001). In addition the calcium channel blocker nicardipine (N) has been administered orally to SHR either chronically during eight weeks (20 mg/kg-1 per os twice daily) or acutely as a single dose of 20 mg/kg. After long term treatment (LT) with N the LVH index and SBP were significantly reduced when compared to vehicle treated (VT) SHR; whereas a single administration of N (AT) only decreased SBP without affecting LVH.(ABSTRACT TRUNCATED AT 250 WORDS)     

Incidence and characteristics of cardiac rhythm disorders after myocardial infarct]

In the course of 1 year 130 patients were examined who had survived myocardial infarction and were alive 2 months after the onset of the disease and were included into the Myocardial Infarction Registry. After 2,3,6,9 and 12 months ECG of various duration was recorded. The prolongation of ECG recording permits to give a more precise characteristics of the incidence and nature of the rhythm disorders observed in chronic ischaemic heart disease patients. Repeated heart rhythm examinations at rest during 1 hour, or during physical exercises (bicycle test) permitted to reveal rhythm disorders in 72.2--66.7% of the patients, and among them ventricular extrasystole in 62.6--66.7% of those examined, respectively. The appearance of ventricular extrasystoles correlates with the state of the patients surviving myocardial infarction A higher incidence of ventricular extrasystoles is observed in pateints with distinct tecg changes, with angina pectoris and elevated blood pressure (larger than or equal to140/90mm Hg).     

Alcohol and rhythm disorders

Cardiovascular disease is the main cause of mortality in chronic alcoholics. There is a clear association between excessive alcohol consumption and the risk of sudden cardiac death. The pro-arrhythmogenic effect of ethanol could be responsible for some of these cases of arrhythmia and sudden death in subjects with an alcoholic cardiomyopathy and also in those with an apparently normal heart. In any case of supraventricular or ventricular arrhythmia in a chronic alcoholic or in an occasional heavy drinker, the potential role of alcohol consumption in the initiation of these disorders should be considered. In all cases, patient management consists of detoxification and abstaining from alcohol consumption, but the withdrawal period is particularly critical as regards the risk of ventricular arrhythmias.     

Hypertensive pregnancy disorders: current concepts

Hypertensive pregnancy disorders complicate 10% of all pregnancies and cover a spectrum of conditions, namely preeclampsia, eclampsia, and chronic and gestational hypertension. Preeclampsia is a pregnancy-specific disorder clinically characterized by hypertension and proteinuria that occurs after 20 weeks of gestation. It remains a leading cause of both fetal and maternal morbidity and mortality worldwide. Traditionally, hypertensive pregnancy disorders were considered not to have any long-term impact on mothers' cardiovascular health; however, recent studies consistently have supported the role of hypertension in pregnancy as a risk factor for cardiovascular disease later in life. Therefore, improved screening, and preventive and treatment strategies may not only optimize management of hypertensive pregnancy disorders, but may have a long-term impact on women's cardiovascular events and outcomes years after the affected pregnancies. This article will provide a brief review of hypertensive pregnancy disorders and important recent discoveries regarding their pathogeneses, while focusing on current diagnostic and treatment strategies.     

Impact and significance of early rhythm disorders after fibrinolytic treatment of myocardial infarction

The study concerns 31 cases of parenteral fibrinolysis performed at the acute stage of myocardial infarction in 30 patients (mean age: 51.9 years), treated less than 4 hours and 15 minutes after the onset of pain. The treatment with streptokinase (80.65%), BRL 26 921 (12.90%) and urokinase (6.45%) was undertaken within a mean time of 3 hours and 17 minutes +/- 53 min. Revascularization defined by the disappearing of pain, the sudden flattening of ST with presence of Q wave, was obtained in 71 p. cent of patients before the 6th hour. The study of the CK curve shows that the enzymatic peak is reached earlier in these patients (13 hours 23 vs 19 h 42). Severe arrhythmias are rare (VF: 0%, transient AVB III: 3.2%). VAIRs were only observed in patients revascularized at an early stage (p 0.02) and in 54.5 p. cent of them. It seems to concern the largest M.Is, treated and revascularized later, regardless of the artery concerned. The syndrome bradycardia-hypotension (Bezold-Jarisch reflex) is only found in patients revascularized at an early stage (22.7 p. cent). Late VES (RR' RR-200 ms or fusion) are more frequent in patients revascularized at an early stage. These three benign rhythm disorders which do not usually require treatment, seem to be good success criteria of fibrinolysis but cannot be considered as predictive indications of myocardial protection.     

Statins and myocardial hypertrophy

Cardiac hypertrophy is a physiological adaptive response by the heart to pressure overload. However, after prolonged periods, this initial adaptive response becomes maladaptive, leading to increased mortality and morbidity from heart failure. Recently, 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, have been shown to inhibit cardiac hypertrophy by cholesterol-independent mechanisms. Statins block the isoprenylation and activation of members of the Rho guanosine triphosphatase (GTPase) family, such as RhoA and Rac1. Since Rac1 is a requisite component of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which is a major source of reactive oxygen species (ROS) in cardiovascular cells, the ability of statins to inhibit Rac1-mediated oxidative stress makes an important contribution to their inhibitory effects on cardiac hypertrophy.     

The laser and rhythm disorders

Of the different types of laser, Nd-YAG radiation (neodymium-yttrium-aluminium-Garnett) is the most suitable for the treatment of arrhythmias. Research in animals has, in fact, made it possible to demonstrate that its properties (high power, creation of a coagulation necrosis without a sectioning effect) may thus be used for the surgical treatment of supra-ventricular tachycardias (Wolff-Parkinson-White syndrome, common flutter, auricular ectopic rhythm) or ventricular tachycardias, the origin of which may or may not be ischemic. Since 1984, it has been possible to treat 25 patients in this way, with good result. In 15 cases, it was a question of curative treatment for a refractory arrhythmia (common flutter: = 1 case, ischemic VT = 12 cases, VT with congenital aneurysm = 1 case). In the other 10 patients the laser was used to prevent an arrhythmia in the course of a CSD (prevention of flutter = 4 cases) or of an aneurysmectomy (6 cases). The excellent results in the short term (the earliest dating back 17 months) lead us to hope that there will be considerable development of the use of the laser in rhythmological surgery.     

Right ventricular myocardial infarction in patients with chronic lung disease: possible role of right ventricular hypertrophy

To determine the relation between right ventricular hypertrophy and right ventricular myocardial infarction in patients with chronic lung disease, the records of 28 patients with chronic lung disease, inferior myocardial infarction and significant coronary artery disease (group I) and 20 patients with right ventricular hypertrophy, chronic lung disease without inferior myocardial infarction or significant coronary artery disease (group II) were reviewed. Chronic lung disease was diagnosed by clinical criteria, chest radiographs and pulmonary function tests. All patients had postmortem examinations. Patients in group I were classified into two subgroups: group Ia (without right ventricular hypertrophy) and group Ib (with right ventricular hypertrophy). Right ventricular wall thickness was 3.3 mm +/- 0.5 in group Ia, 6.0 mm +/- 1.1 in group Ib and 8.8 mm +/- 2.4 in group II (group Ia versus Ib, p less than 0.001; group Ia versus II, p less than 0.001; group Ib versus II, p less than 0.001). Eleven patients (78.6%) in group Ib (chronic lung disease with both right ventricular hypertrophy and inferior myocardial infarction) had right ventricular myocardial infarction compared with only 3 patients (21.9%) in group Ia (chronic lung disease without right ventricular hypertrophy and with inferior myocardial infarction) (p less than 0.008). Isolated right ventricular myocardial infarction occurred in four patients (20%) in group II (chronic lung disease with right ventricular hypertrophy, but without evidence of infarction of the left ventricle or significant coronary artery disease). There was no significant difference in the extent of anatomic coronary disease in groups Ia and Ib.(ABSTRACT TRUNCATED AT 250 WORDS)