Osteoprotegerin is a significant prognostic factor for overall survival in patients with primary systemic amyloidosis independent of the Mayo staging.

Bone metabolism has not been systematically studied in primary (AL) amyloidosis. Thus we prospectively evaluated bone remodeling indices in 102 patients with newly diagnosed AL amyloidosis, 35 healthy controls, 35 newly diagnosed myeloma and 40 monoclonal gammopathy of undetermined significance patients. Bone resorption markers (C-telopeptide of type-1 collagen, N-telopeptide of type-1 collagen) and osteoclast regulators (soluble receptor activator of nuclear factor-κB ligand (sRANKL), osteoprotegerin (OPG)) were increased in AL patients compared with controls (P<0.01), but bone formation was unaffected. Myeloma patients had increased bone resorption and decreased bone formation compared with AL patients, while sRANKL/OPG ratio was markedly decreased in AL, due to elevated OPG in AL (P<0.001). OPG correlated with N-terminal pro-brain natriuretic peptide (P<0.001) and was higher in patients with cardiac involvement (P=0.028) and advanced Mayo stage (P=0.001). OPG levels above the upper value of healthy controls was associated with shorter survival (34 versus 91 months; P=0.026), while AL patients with OPG levels in the top quartile had very short survival (12 versus 58 months; P=0.024). In Mayo stage 1 disease, OPG identified patients with poor survival (12 versus >60 months; P=0.012). We conclude that increased OPG in AL is not only a compensation to osteoclast activation but may also reflect early cardiac damage and may identify patients at increased risk of death within those with earlier Mayo stage.

Impact of cardiac transplantation in 24 hours circadian blood pressure and heart rate profile.

OBJECTIVE: The aim of the present study was to evaluate 24 hours blood pressure (BP) and heart rate changes as well as 24-hour circadian BP rhythm of cardiac transplant recipients. METHODS: Twenty-five transplant recipients and twenty-five healthy volunteers underwent 24-hour ambulatory BP monitoring. Parameters of 24-hour ambulatory BP monitoring (24-h/daytime/nightime systolic, diastolic BP, pulse pressure, and heart rate) were determined in all patients. RESULTS: Clinic systolic/diastolic BP, mean 24-h systolic/diastolic BP, mean daytime systolic/diastolic BP, mean nighttime systolic/diastolic BP, and mean 24-h/daytime/nighttime heart rate were significantly higher in transplant recipients than in control group subjects. Standard deviations of 24-h/daytime/nighttime heart rates were significantly lower in transplant recipients. Dippers were 48% of the control and only 12% of the transplantation group. CONCLUSIONS: Cardiac transplant recipients had increased ambulatory BP. They also had increased 24-h/daytime/nighttime heart rate and decreased heart rate variability. Also, diminished nocturnal decrease of BP was found in transplant recipients.

Pulse pressure in normotensives: a marker of cardiovascular disease.

The purpose of the present study was to evaluate the relation of the systemic arterial pulse pressure and other parameters derived from the 24-h arterial blood pressure (BP) monitoring to the severity of coronary artery disease, carotid lesions, and left ventricular (LV) mass index in patients without arterial hypertension. One hundred ten patients with known coronary artery disease underwent coronary arteriography, 24-h arterial BP monitoring, and ultrasound imaging of the carotid arteries and the myocardium. Measurements of 24-h arterial BP monitoring (systolic, diastolic, and average BP, pulse pressure, abnormal values of systolic and diastolic BP, and heart rate), the severity of coronary heart disease (Gensini score), intima-media thickness (IMT) of the common carotid artery and LV mass index were determined in all patients. By univariate analysis, only 24-h pulse pressure was significantly related to the severity of coronary artery disease (P < .01), carotid IMT(P < .01), and LV mass index (P < .01). In a multivariate analysis, 24-h pulse pressure was also the best predictor of the severity of coronary lesions (P = .009), carotid IMT (P = .003), and LV mass index (P = .009). Gensini score was related (P < .01) to LV mass index and not to carotid IMT. In conclusion, systemic arterial pulse pressure derived from 24-h arterial BP monitoring is related to coronary artery disease, carotid IMT, and LV mass index independently of age or any other derivative of 24-h arterial BP monitoring, indicating that this parameter could be a marker of global cardiovascular risk.

Indium-111 monoclonal antimyosin cardiac scintigraphy in men with idiopathic dilated cardiomyopathy.

This study examined the prognostic value and the evolution of the heart-to-lung ratio of monoclonal antimyosin antibody (MAA) uptake in patients with a diagnosis of idiopathic dilated cardiomyopathy (IDC). Uptake of indium-111-labeled MAA occurs when the myocytes become irreversibly damaged. The study included 29 men with IDC followed up for 3 years. The diagnosis was verified by endomyocardial biopsy in all patients. Patients who survived beyond 1 year were restudied. Baseline heart-to-lung ratio of MAA was 1.74+/-0.22. Multivariate Cox regression analysis revealed that MAA and New York Heart Association class were independent predictors of late mortality, with a hazard ratio of 4.4 (95% confidence interval 1.1 to 17.9, p = 0.036) and 7.5 (95% confidence interval 2.0 to 28.4, p = 0.003), respectively, when heart-to-lung ratio of MAA uptake was > 1.74 and New York Heart Association class was >11. When these patients were divided into those with chronic IDC (group I [n = 19]) and those with subacute IDC (group II [n = 10]), baseline heart-to-lung ratio was 1.7+/-0.2 and 1.86+/-0.25, respectively (p = NS). In the surviving patients, on restudy, the heart-to-lung ratio of MAA uptake was unchanged in group I (1.64+/-0.20, p = NS), but had decreased to the level of group I (1.66+/-0.21 [p = 0.008]) in group II. Thus, men with IDC and a high heart-to-lung ratio of MAA uptake have a worse long-term prognosis than patients with a lower ratio. The heart-to-lung ratio of MAA decreases comparably over time in subacute IDC and remains stable in chronic IDC.

A pressure-time index' for assessing the severity of essential hypertension.

OBJECTIVE: A new derivative of 24 h ambulatory blood pressure monitoring (ABPM) is introduced and its association with left ventricular mass index (LVMI) in essential hypertension is examined. PATIENT: population One hundred and fifty-three previously untreated essential hypertension patients. METHODS: Patients underwent casual blood pressure (BP) readings, 24 h ABPM and left ventricular echocardiographic assessment The following 24 h awake and sleep ABP variables were calculated: mean systolic and diastolic BP, systolic and diastolic BP loads (percentage of systolic readings > 140/120 mmHg (day/ night) and diastolic readings > 90/80 mmHg (day/night)), standard deviation of systolic and diastolic ABP and nocturnal fall of systolic BP, as well as the integrated areas under the ABP curve. The area under the BP curve divided in horizontal slices was accurately modelled by a sigmoid curve. The parameters controlling the shape of the curve and in particular that regarding its 'slope' is hereafter called the 'pressure-time index'. RESULTS: 'Systolic pressure-time index 24 h' (SPTI24) is related to left ventricular mass index (multivariate analysis, P= 0.008). Using either partial correlation coefficients or a multivariate analysis, SPTI24 is related to left ventricular mass index, independently of age, casual blood pressure, mean systolic and diastolic ABP, systolic and diastolic BP loads, BP variability (standard deviation (SD), nocturnal fall of systolic BP) and integrated area under the curve (multivariate analysis, P= 0.004). CONCLUSIONS: In essential hypertension, the SPTI24 is related to LVMI independently of age, casual blood pressure, integrated area under the curve or any other derivative of 24 h ABPM, and might be used to assess the extent of hypertensive load.

Detection of coronary artery disease in the presence of left ventricular atrophy.

To evaluate the accuracy of exercise echocardiography for the recognition of coronary artery disease in the presence of left ventricular hypertrophy 70 patients were studied. Significant coronary artery disease was present in 25 patients and left ventricular hypertrophy had 29 patients. All patients underwent an exercise ECG and echocardiographic test during which cine-loop digitized echocardiography was obtained. Wall motion was analyzed and a regional wall motion score index was calculated. The overall sensitivities of exercise ECG and echocardiography for detecting coronary artery disease were 60% and 64%, respectively, and the specificities were 49% and 78%, respectively. In patients with left ventricular hypertrophy the specificity of exercise echocardiography was higher (71%) compared to exercise ECG (21%) while in patients without hypertrophy the sensitivity was higher (70% vs. 40%, respectively). Of the 19 patients with a non-diagnostic stress ECG, echocardiography correctly identified 100% of those with coronary artery disease but only 53% of those without disease. It is concluded that exercise digital echocardiography represents a good diagnostic alternative to the exercise ECG for identifying coronary artery disease in the presence of left ventricular hypertrophy and should be useful in patients with a non-diagnostic exercise ECG.

Atrial pressure and experimental atrial fibrillation.

A possible profibrillatory effect on the atria of an elevated atrial pressure and the site of atrial stimulation was examined. In 15 anesthetized dogs, right or left atrial or biatrial pacing was applied at a high rate (300-600/min) for 5 seconds at double threshold intensity under a wide range of atrial pressures achieved by venous or arterial transfusion or bleeding. Induction of atrial fibrillation in 236 of 1,971 pacing runs was associated with a significantly higher (P < 0.001) atrial pressure (21.6 +/- 12.2 mmHg, mean +/- SD) than maintenance of sinus rhythm (16.8 +/- 11.1 mmHg in 1,735 of 1,971 pacing runs). Stimulation of the right atrium resulted in atrial fibrillation more frequently than left atrial or biatrial stimulation, with biatrial stimulation less frequent than right or left atrial stimulation. The induction of atrial fibrillation was related to the atrial pressure and to the site of stimulation but not to the pacing rate or the prepacing heart rate. The prepacing heart rate, associated with failure to induce sustained atrial fibrillation, was higher than that associated with atrial fibrillation in 12 of 15 experiments (significantly in 6) and not significantly lower in 3 of 15. Atrial fibrillation lasting 1 minute or more was more frequently associated with simultaneous stimulation of both atria than of either atrium alone. Thus, an elevated atrial pressure may facilitate the induction of atrial fibrillation. The site of stimulation also plays an important role for both the induction and maintenance of atrial fibrillation in this model.

Cardiac involvement in collagen diseases.

The purpose of this study is to evaluate the early morphological and functional abnormalities of the heart in patients with collagen disease. The study population was free of risk factors for coronary artery disease and without any clinically evident cardiac manifestations. In 62 patients with collagen disease (25 with progressive systemic sclerosis, 19 with systemic lupus erythematosus, 15 with rheumatoid arthritis, three with dermatomyositis) and in 40 healthy subjects an echocardiographic study was performed. Echocardiographic examination from the apical four-chamber view was performed at rest and during the end of a 3 min isometric exercise with handgrip. Global and regional ejection fraction of the left ventricle were calculated. In the group with progressive systemic sclerosis the left ventricular mass index was significantly higher than in the control group (110.78 +/- 48.61 vs 82.18 +/- 28.46 g.m-2) and the ejection fraction (53.61 +/- 7.95%) was the lowest of all groups (control: 61.47 +/- 8.52%, systemic lupus erythematosus: 59.04 +/- 8.58%, rheumatoid arthritis: 62.38 +/- 6.88%). Regional ejection fraction analysis revealed a major dysfunction of the proximal segment of the interventricular septum, in all groups. During isometric exercise, the global and regional ejection fraction did not change significantly, although differences between groups disappeared. In rheumatoid arthritis, mitral and aortic valve leaflet separation appeared to be reduced. In the group with systemic lupus erythematosus, mild abnormalities were noticed, although the mean age and duration of the disease were the smallest compared with the other groups. In conclusion, patients with progressive systemic sclerosis mainly present left ventricular hypertrophy with a reduced ejection fraction while rheumatoid arthritis patients show a predominant valve dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Some observations on the mechanism of pressure related atrial fibrillation.

In order to investigate the effect of atrial pressure on the propensity of the atria to fibrillate and the mechanism of this association, the right atrial pressure was changed acutely by transfusion-bleeding in 12 anaesthetized open-chest dogs. Under various atrial pressures the conduction time was measured between two pairs of hook electrodes positioned on the two atrial appendages respectively. The effective refractory period was measured by continuous pacing of the right atrium at a 250 ms cycle length at double threshold intensity and interpolating a progressively earlier stimulus after each eighth paced beat. The propensity of fibrillation was studied by rapid (450 min-1) pacing of the atria at double threshold intensity for 10 s at different atrial pressures. At a high (> or = 14 mmHg) atrial pressure the conduction time (45.7 +/- 14.2 ms) was significantly (P < 0.01) longer, the effective refractory period (157.9 +/- 15.2 ms) significantly (P < 0.01) longer and the atrial fibrillation (11/19 or 57.9%) significantly (chi 2 = 9.95, P < 0.001) more common than at a low (< or = 10 mmHg) pressure (35.2 +/- 11.6, 146.2 +/- 12.4, 3/24 or 12.5%, respectively). Analysis of variance showed that the probability of atrial fibrillation was significantly affected by the atrial pressure but not by either the conduction time or the effective refractory period. The findings suggest that an increase in right atrial pressure by acute volume overload prolongs the inter-atrial conduction time and right atrial refractoriness and increases the propensity of the atria to fibrillate by rapid atrial stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of acute ventricular pressure changes on QRS duration.

The effect of acute changes in ventricular pressure is examined on the QRS duration to clarify the mechanism of ventricular pressure-related arrhythmogenesis. Ventricular pressure was changed acutely by arterial transfusion-bleeding into an open-air ventricular pressure reservoir that was either off or on a metaraminol intravenous drip. While maintaining ventricular pressure at several levels, the QRS duration was measured at 200 mm/s paper speed. The QRS duration correlated significantly with the left ventricular pressure in all 14 dogs examined. An average change in ventricular by 100 mmHg was associated with a change of about 18% in the QRS duration. An acute ventricular pressure elevation impairs the ventricular conduction, which may contribute to ventricular pressure-related arrhythmogenicity.

Acute effects of external and internal pacing on ejection fraction in patients with severe cardiac failure.

The present study aims at evaluating the acute hemodynamic effects of external and internal (3 and 15 mA) pacing on 30 patients with severe cardiac failure. The global and regional ejection fraction were calculated by repeated radionuclide ventriculography at rest (control) and during increasing pacing rates. Blood pressure was measured at the end of each scintigraphy data acquisition period. The pacing rate was increased by 10 beats/min in every step and varied between +10 to +60 beats/min above the resting heart rate. The ejection fraction during pacing was lower than the resting ejection fraction in every pacing mode (resting ejection fraction = 23.30 +/- 7.67%, external pacing = 19.36 +/- 9.30%, p < 0.05, internal pacing 3 mA = 22.15 +/- 7.00%, p = N.S., internal pacing 15 mA = 19.92 +/- 6.95%, p < 0.05). The resting ejection fraction was higher than the ejection fraction in every pacing rate. In 4 out of 30 patients the ejection fraction was higher in every pacing mode and rate than the resting ejection fraction. The regional ejection fraction of the interventricular septum during internal pacing was lower (p < 0.001) than resting and/or external pacing. In conclusion, pacing in patients with severe cardiac failure reduces the control ejection fraction. This reduction increases as the pacing rate increases. The reduction is greater with internal pacing of 15 mA while the hemodynamic effect in external pacing did not differ significantly from internal pacing. Overall, the resting ejection fraction was higher than the paced ejection fraction, although in some patients pacing improved their resting ejection fraction.

Effect of acute blood pressure changes on signal averaged electrocardiogram.

An acute blood pressure elevation may cause ventricular ectopic rhythms, while its reduction may alleviate them. It is studied whether the blood pressure exerts some effect on parameters obtained by the signal averaged electrocardiogram. In 25 patients with either hypertension (8 cases) or ventricular ectopic rhythms (10 cases) or both (7 cases) the blood pressure was reduced by sodium nitroprusside (24 cases) and/or elevated with metaraminol (10 cases) and the signal averaging electrocardiogram was recorded under 2 or 3 pressure values on each patient. During the high pressure (193.6 +/- 20.1 mm Hg) the following differences were noted compared to the low pressure (77.4 +/- 15.2 less): longer QRS duration in all 25 patients (+9.92 +/- 10.51 ms, P < 0.001); longer low (< 40 microV) amplitude signals (LAS) in 18 patients (+6.94 +/- 10.93 ms, P < 0.005); lower root mean square voltage of the terminal 40 ms of the QRS in 22 patients (-15.73 +/- 21.60 microV, P < 0.005); and ventricular ectopic beat incidence higher in 8, lower in 1, and equal in 2 cases (with no arrhythmia in the other 14). The generally and focally reduced conduction, as suggested by the QRS and LAS prolongation, might contribute to the proarrhythmic effect of acute blood pressure elevation.

Anatomical origin of pressure-related ventricular ectopic rhythms.

In order to determine the origin of pressure-related ectopic rhythms, the main arteries were clamped in 11 anesthetized dogs, or the arteries or veins were transfused, while on or off metaraminol. The epicardial right atrial electrogram, the intracavity electrograms and the pressure of the two ventricles were recorded. Sinus rhythm was associated with 64/64 (100%) of the control periods off metaraminol, but only 19/50 (38%) of the clamping of the main arteries (P << 0.0005). In 14/27 aortic clampings ectopic beats appeared from the left ventricle and in 13/27 from the right one. In 4/23 clampings of the pulmonary artery ectopic beats appeared from the left ventricle and in 15/23 from the right one (P < 0.05). Sinus rhythm was associated with significantly lower left ventricular systolic pressure than any ventricular arrhythmia. The left ventricular systolic pressure associated with ectopic rhythms from the left ventricle was significantly (P < 0.005) higher than that associated with those from the right ventricle. The right ventricular systolic pressure during sinus rhythm was significantly (P < 0.005) lower than that during ectopic rhythm from any ventricle. It is concluded that a rise in the pressure of one ventricle tends to cause ventricular ectopic rhythms originating predominantly, but not exclusively, from this ventricle. The origin of ventricular ectopic rhythms from the right ventricle does not preclude that the arrhythmia may respond favorably to lowering of the systemic pressure.

The role of mitral annulus motion in left ventricular function.

The dynamics between mitral annulus motion and left ventricular function were studied. Thirty subjects (10 normals, 10 with severe cardiac failure and 10 with mitral regurgitation) were examined. Left ventricular long and short-axis dimensions were measured in a two-dimensional apical four-chamber image. A volume was calculated as defined by cardiac cyclic changes of mitral annulus in size and motion. This volume had the approximate geometric configuration of a truncuated cone and was covered by mitral annulus motion at enddiastole and endsystole. Left ventricular ejection fraction was calculated echocardiographically using the prolate ellipsoid/area-length method. The volume defined by mitral annulus motion was 24 ml in normals, 16 ml in patients with cardiac failure and 48 ml in patients with mitral regurgitation while the ejection fraction was 51%, 19% and 53% respectively. Comparison between the volume of the truncuated cone and the ejection fraction in all 30 subjects revealed a statistically significant correlation (p less than 0.01). Thus, the bigger the volume determined by the mitral annulus motion during systole, the larger portion of the left ventricle is "atrialized", and a higher ejection fraction follows. Mitral annulus motion may provide new information about cardiac mechanics in normal and abnormal conditions.

The circadian profile of extrasystolic arrhythmia: its relationship to heart rate and blood pressure.

This paper aims at examining whether there is an association between the circadian patterns of systolic blood pressure, heart rate and the incidence of ventricular ectopic beats, as well as to confirm that reducing the blood pressure by a diuretic may also reduce the ectopic frequency. Thirty-four ambulatory patients with ventricular ectopic beats and a systolic blood pressure of 131.33 +/- 17.46 mmHg had a 24-hour Holter electrocardiographic and blood pressure monitoring following 1 week off any antiarrhythmic and antihypertensive treatment. Then they received for one week a standard diuretic combination (amiloride 5 mg + hydrochlorothiazide 50 mg) at a dose depending on their systolic pressure value and their monitoring was repeated. The mean hourly values of systolic blood pressure, heart rate and ventricular ectopic beats were "normalized", i.e. expressed as (x-x)/SD, taking each patient's 24-hour average as zero and his own standard deviation as the unit of measurement. As a group, there was an independent positive correlation between blood pressure and ectopic beats, while the heart rate was a nonsignificant negative factor for ectopic beats. On an individual level, however, an independent positive significant correlation between blood pressure and ectopic beats was found in only 8 cases, with a negative one in 4 cases. While the blood pressure of the group ranged symmetrically around its daily average value, the corresponding ectopic beat curve was highly asymmetric, with a very high incidence (up to 2.56 +/- 0.52 SD) for a rather short time (only 9.41 +/- 3.56 hours above average) and a low incidence (up to 1.26 +/- 0.49 SD) for the remaining 14.59 hours below average. Sudden rises in ectopic beat (greater than 1 SD/hour) occurred 1 to 6 times per day in each individual, significantly (P less than 0.01) more often (20.31%) with a high (greater than 1 SD) blood pressure than with a low (less than -1 SD) one (8.99%) with intermediate frequencies at intermediate pressures. After treatment with the diuretic, the systolic blood pressure was reduced, the heart rate increased and the ventricular ectopic beat incidence reduced (significant changes). The mean change in systolic pressure in 25 patients with a reduction in ectopy was a significant (P less than 0.01) decrease (-5.21 +/- 8.70 mmHg) while in the remaining 9 cases there was a non significant increase (+1.68 +/- 7.63 mmHg). The heart rate was higher in both subgroups.(ABSTRACT TRUNCATED AT 400 WORDS)

Induced electrophysiological isolation of the myocardium prevents ventricular fibrillation.

STUDY OBJECTIVE: to investigate whether an encircling procedure without ventriculotomy, not involving the endocardium, may have a protective effect against ventricular fibrillation (VF), by achieving a physiological rather than anatomic entrenchment. DESIGN: the occurrence of VF was tested by DC application within an area entrenched by a circular "dotted" line formed by LASER (Nd-Yag) point by point applications. The result was compared with that from similar DC applications before the successful LASER entrenchment or beyond the restricted area. SUBJECTS: 16 anaesthetized mongrel dogs, weights 14-20 kg were used. MEASUREMENTS AND RESULTS: VF occurred 13/118 times by applying DC within the entrenched area and 86/114 times by applying the current outside this area or before the intervention (P less than 0.0005). The pacing threshold was significantly (P less than 0.001) increased within the circumscribed area (4.625 +/- 5.335 vs 0.859 +/- 0.947 mA). The maximal rate at which the ventricles could be driven by pacing at double threshold intensity was not significantly altered by the encircling procedure. Histological examination showed crater-like epicardial destruction with necrosis, loss of myocardial striation, haemorrhage, and polymorphonuclear infiltration, extending about 0.5 cm from the necrotic tissue. The subendocardial area was spared showing only hyperaemia, while the endocardium was intact. CONCLUSIONS: Encircling a small area by LASER point by point applications prevents the occurrence of VF when DC is applied within the restricted area, while permitting the conduction of paced beats. The size of the encircled area necessary to this effect is of importance, possibly reflecting the critical mass needed for the occurrence and maintenance of VF.

Effect of adrenergic blockade on pressure-related ventricular arrhythmias.

This paper examines whether adrenergic blockade (B1) may prevent the arrhythmogenic effect of acute arterial pressure (AP) elevation. In 7 anesthetized dogs iv propranolol (0.2 mg/kg) was given and in another 2 dogs stellate ganglion excision was performed. Before and after these B1 manoeuvres the AP was repeatedly increased by either elevating an open-air arterial pressure reservoir or administering iv metaraminol and decreased by abating the pressure reservoir. In a continuous recording of AP and ECG the systolic (S) AP and the presence (or absence) of ventricular arrhythmia (A) was noted. Before B1 A was noted in 652/1715 (38.0%) 5-sec periods at a SAP of 160.3 +/- 69.9 mm Hg which was significantly higher than in the 1063 5-sec periods without A (104.2 +/- 54.3) in all experiments. Following B1 it was impossible to cause A in 3 experiments. In the remaining experiments the A incidence was reduced (significantly in 5/9 experiments) to a total of 253/983 (25.7%) periods (P less than 0.001). In the 5/9 experiments with post-B1 A, the mean SAP was higher with (185.0 +/- 97.9 mm Hg) than without A (113.7 +/- 59.9 mm Hg) (significantly in 2/9 experiments). Following fitting of the SAP distributions before and after B1 to their common distribution (i.e. the same AP), the incidence of A was higher before than after B1 in all experiments (significantly in 7/9). It is concluded that B1 has an antiarrhythmic action on AP-related A. This antiarrhythmic effect seems to be due partly to an antihypertensive effect of B1 and partly to an antiarrhythmic effect of B1 for a given AP.

Effect of 24-hour blood pressure and heart rate variations on left ventricular hypertrophy and dilatation in essential hypertension.

This study correlates variables derived from blood pressure (BP) and heart rate (HR) monitoring with the degree of left ventricular structural changes in essential hypertension. Forty patients with mild-to-moderate hypertension according to World Health Organization criteria underwent 24-hour ambulatory monitoring. Echocardiographic (posterior wall and interventricular septum thickness, left ventricular mass) or ECG (SV1 + RV5) indices of hypertrophy were significantly (p less than 0.01) correlated (positive correlations) with derivatives of BP monitoring (mean systolic and diastolic BP values) but not with HR derivatives. Echocardiographic indices of dilatation (left ventricular end-diastolic volume and diameter) were significantly (p less than 0.01 to less than 0.001) correlated (negative correlations) with derivatives of HR monitoring (mean HR values, mainly during the night) but not with BP derivatives. It is concluded that in essential hypertension, left ventricular hypertrophy depends on mean 24-hour systolic and diastolic BP values, whereas left ventricular dilatation appears to be more prominent in patients with bradycardia mainly during the night.

Response of tertiary centres to pressure changes. Is there a mechano-electrical association?

STUDY OBJECTIVE: To investigate the mechanism of pressure related ventricular arrhythmias by examining them during atrioventricular (AV) block. DESIGN: Complete AV block, where all ventricular beats are ectopic, was induced by AV node ablation and/or by toxic digitalisation, and rhythm changes were studied while arterial blood pressure was repeatedly raised and lowered. SUBJECTS: 15 anaesthetised mongrel dogs, weight 15-28 kg, were used. AV block was induced in eight by chemical or mechanical ablation of the AV node. In five of these and in seven other dogs, 5.0-7.5 mg digoxin was also given. MEASUREMENTS AND RESULTS: Following AV block due to ablation, a heart rate increase (or no change) was found in 87.5% of 56 arterial pressure increases produced by elevation of an open arterial blood reservoir or by metaraminol infusion, but in only 21.8% of 55 pressure decreases caused by arterial bleeding (p much less than 0.001). Following AV block due to digitalisation, the equivalent figures were 96% of 50 pressure increases and 27.3% of 55 pressure decreases (p much less than 0.001). While arterial pressure was increased there was moderate acceleration of the escape rhythm, then appearance of premature ventricular beats, then non-sustained and finally sustained ventricular tachycardia. The reverse occurred, with some hysteresis, on decreasing the arterial pressure. In five of the digitalised animals, arterial pressure reduction to nearly zero caused reproducible sudden arrest, with resumption of the ordinary escape rhythm on increasing the pressure again. CONCLUSIONS: The findings suggest the possibility of two kinds of ectopic rhythm in AV block: the "normal" escape rhythm which is only moderately affected by arterial pressure changes; and an "abnormal" faster pressure dependent rhythm which is generated by high arterial pressure and abolished by pressure near zero, as if there were a mechano-electrical association. This abnormal rhythm may prevail completely in digitalis toxicity so that if cardiac arrest occurs, no automaticity can be expected to appear unless arterial pressure is raised.