Complete atrioventricular block with unwidened QRS complex during hyperkalemia.

Purkinje and ventricular myocardial fibers are thought to be more sensitive to hyperkalemia than sinoatrial and atrioventricular (AV) nodes, although complete AV block due to hyperkalemia can occur. We describe a case in which hyperkalemia in a patient affected by renal failure is responsible for complete AV block without QRS complex prolongation. Temporary endoventricular pacing was essential in restoration of adequate renal blood flow and excretion of exceeding serum potassium with subsequent normalization of AV conduction.

Systemic thrombolysis for acute myocardial infarction in a renal transplant recipient.

This study describes the successful management of an acute myocardial infarction occurring in a renal transplant recipient with thrombolytic therapy. Although primary coronary angioplasty has been addressed as an alternative therapeutic approach, this approach raises concern for angiography-related contrast media renal toxicity. However, pharmacological therapy with thrombolytics is effective and relatively safe and should be considered as the first-choice treatment in today's clinical setting.

[Isolated cardiac amyloidosis. Presentation of a clinical case]. / Amiloidosi cardiaca isolata.

A 48-year old patient affected by congestive heart failure came to our observation for cardiac arrest due to ventricular fibrillation. After cardiopulmonary resuscitation and defibrillation he underwent complete evaluation. Echo Doppler findings were consistent with restrictive cardiomyopathy. Laboratory findings revealed monoclonal gammopathy and plasma cells dyscrasia. Diagnosis of amyloidosis was then suspected and biopsies of different organs and tissues were performed. Presence of amyloid deposits was found only in myocardial specimens from the right ventricle. Medical treatment with drugs of various classes, administered during hemodynamic invasive monitoring, was uneffective in improving the hemodynamic and clinical status of the patient and he entered in a heart transplantation list. He died six months later, while awaiting for transplantation. Although isolated cardiac amyloidosis is quite rare, we believe that this condition has ever to be kept in mind during differential diagnosis of restrictive cardiomyopathies and we remark that endomyocardial biopsy was mandatory and necessary for certain diagnosis in this case; in addition, the unefficacy of drugs nowadays available for treatment of congestive heart failure in amyloid cardiomyopathy is confirmed.

Clinical, electrocardiographic, and echocardiographic features in patients with asymptomatic aortic abdominal aneurysm.

Cardiac involvement in peripheral vascular diseases can present interesting patho-physiological aspects and can influence the prognosis. The authors evaluated the cardiac condition of patients with asymptomatic aortic abdominal aneurysm (AAAA) by using clinical, electrocardiographic, and echocardiographic techniques. Seventy-eight patients were studied, 74 men and 4 women, with ages ranging from fifty-five to eighty-one years (mean 69.5 +/- 6.4). All patients were submitted to a complete clinical examination, usual blood tests, a 12-lead resting electrocardiogram, and an echo-Doppler evaluation. Forty-eight subjects (61.5%) were affected by hypertension, 53 (67.9%) were smokers, 25 (32.1%) were alcohol abusers, 39 (50%) had a history of angina pectoris, 20 (25.6%) had had previous myocardial infarction, and 30 (38.5%) were receiving active cardiovascular treatment. All patients except 2, who had chronic atrial fibrillation, manifested sinus rhythm. Electrocardiographic signs of left ventricular (LV) hypertrophy were present in 20 cases (25.6%), intraventricular conduction disturbances in 19 (24.4%), pathological Q waves in 20 (25.6%), and primary repolarization abnormalities in 25 (32.1%). Echocardiography showed a slight increase in left atrial diameter and intraventricular septum thickness (41.5 +/- 4.3 and 12.3 +/- 2 mm respectively). A clearer increase was found in LV mass index (159 +/- 44 g/m2). In 31 patients one or more LV asynergic segments were found. In our patients with AAAA the prevalence of major risk factors for atherosclerosis and ischemic heart disease including previous myocardial infarction was high. Echo-derived LV myocardial mass index was higher than normal even though electrocardiographic criteria for LV hypertrophy did not match echocardiographic data in all subjects. Finally a moderate prevalence of intraventricular conduction disturbances was recorded.

Left-ventricular outflow tract obstruction by mitral valve ring calcification and proximal septal hypertrophy in elderly patients. Presentation of 2 clinical cases.

The pathophysiology, clinical presentation and prognosis of left-ventricular obstruction still represent an important cardiological problem. Various anatomical and/or functional mechanisms can cause this phenomenon. This report concerns 2 patients over 75 years old in whom the simultaneous presence of localized proximal septal hypertrophy and massive calcification in the anterior portion of the mitral valve ring provoked significant systolic intraventricular gradients. Cardiac rhythm disturbances and consequent variability of R-R intervals, found in both subjects, appear fundamental in determining the value of such gradients. Occasionally an anterior mitral ring calcification may bring about left-ventricular outflow tract obstruction in aged hearts where localized hypertrophy of the proximal portion of the intraventricular septum is present.

Effect of aging on left ventricular filling in untreated hypertensive patients.

The aim of this study was to evaluate the influence of age and other clinical and echocardiographic parameters on left ventricular filling in a group of 174 untreated patients with mild to moderate hypertension (aged 20-82 years; mean 51.2 years) and in 189 age-matched normotensive subjects. All subjects underwent an echocardiographic study with pulsed Doppler evaluation of left ventricular filling. Left ventricular dimensions and indexes of systolic function were similar and within normal limits in both groups. Left ventricular filling was altered in hypertensive subjects < 65 years with a decrease of peak early velocity (peak E), an increase of peak atrial velocity (peak A) and a reduced E/A ratio. However in subjects > or = 65 years, we did not observe any differences in transmitral flow velocity pattern between hypertensive and normotensive subjects. The stepwise regression analysis showed that age alone explains up to 8% of peak E variance, 14% of peak A and 26% of E/A ratio in hypertensives, while in normotensives it explains up to 18% of peak E variance, 50% of peak A and 61% of E/A ratio. The other variables entered into the regression slightly improved the predictive power. In conclusion, age is the major independent factor affecting left ventricular filling in both groups, even if its predictive power was smaller in the hypertensive group. The similarity of diastolic filling pattern in elderly hypertensive and normotensive subjects suggests that the 'aging factor' plays an important role in influencing left ventricular filling pattern so as to mask the effect of hypertension in the elderly patients.

[Cardiac and skeletal malformations in a 55-year-old man. Holt-Oram syndrome]. / Anomalie cardiache e scheletriche in cinquantacinquenne. Sindrome di Holt-Oram.

A patient with Holt-Oram syndrome, diagnosed in advanced age, in which skeletal anomalies of upper limbs and clavicles are associated with ostium secundum atrial septal defect, great left-to-right shunt and marked pulmonary hypertension is described. The importance of a prompt interdisciplinary instrumental diagnostic approach is underlined.

Myocyte cellular hypertrophy and hyperplasia contribute to ventricular wall remodeling in anemia-induced cardiac hypertrophy in rats.

To determine the effects of chronic anemia on the functional and structural characteristics of the heart, 1-month-old male rats were fed a diet deficient in iron and copper, which led to a hemoglobin concentration of 4.63 g/dl, for 8 weeks. At sacrifice, under fentanyl citrate and droperidol anesthesia, systolic, diastolic, and mean arterial blood pressures were decreased, whereas differential pressure was increased. Left ventricular systolic pressure and the ventricular rate of pressure rise (mmHg/s) were reduced by 9% and 14%, respectively. Moreover, developed peak systolic ventricular pressure and maximal dP/dt diminished 14% and 12%. After perfusion fixation of the coronary vasculature and the myocardium, at a left ventricular intracavitary pressure equal to the in vivo measured end diastolic pressure, a 10% thickening of the left ventricular wall was measured in association with a 13% increase in the equatorial cavitary diameter and a 44% augmentation in ventricular mass. The 52% hypertrophy of the right ventricle was characterized by an 11% thicker wall and a 37% larger ventricular area. The 33% expansion in the aggregate myocyte volume of the left ventricle was found to be due to a 14% myocyte cellular hypertrophy and a 17% myocyte cellular hyperplasia. These cellular parameters were calculated from the estimation of the number of myocyte nuclei per unit volume of myocardium in situ and the evaluation of the distribution of nuclei per cell in enzymatically dissociated myocytes. Myocyte cellular hyperplasia provoked a 9% increase in the absolute number of cells across the left ventricular wall. In contrast, myocyte cellular hypertrophy (42%) was responsible for the increase in myocyte volume of the right ventricle. The proliferative response of left ventricular myocytes was not capable of restoring diastolic cell stress, which was enhanced by the changes in ventricular anatomy with anemia. In conclusion, chronic anemia induced an unbalanced load on the left ventricle, which evoked a hyperplastic reaction of preexisting myocytes, in an attempt to normalize diastolic wall and myocyte stress.