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Although several independent studies have claimed a link between Helicobacter pylori infection and coronary heart disease (CHD), this association has not been established conclusively. The aim was to determine whether an association between H. pylori infection and CHD can be demonstrated in Japanese patients. Three-hundred and four patients who underwent consecutive coronary arteriography were investigated. Ninety-four patients had single-vessel coronary stenosis and 112 had multi-vessel stenosis. The remaining 98 patients had no significant stenosis in any coronary arteries. H. pylori infection was diagnosed serologically and the association between infection and CHD was estimated by the odds ratio. The serum pepsinogen (PG) I-II ratio was used to estimate the degree of gastric atrophy. Seropositivity for H. pylori was significantly higher in the patients with CHD (67%) than in the controls (50%; p = 0.006). The odds ratio for CHD after having H. pylori infection was estimated as 1.35 (95% confidence interval 1.03–1.78; p = 0.028), after adjustment for the common risk factors of CHD in a logistic regression analysis. The association between CHD and H. pylori infection was more significant among patients without any history of diabetes or smoking. The PG I-II ratio in H. pylori-positive patients was significantly higher in the multi-vessel group (3.46) than in the control or single-vessel group (2.86, p = 0.030; 2.78, p = 0.008; respectively). H. pylori infection was shown to be an independent risk factor for CHD in Japanese patients, especially among those who did not have a history of diabetes or smoking. These data imply that the association between H. pylori infection and CHD is clinically relevant.

A total of 502 patients presenting in Utsunomiya city and its suburbs during a 10-year period were studied to determine the clinical features of ischemic heart disease and to identify coronary risk factors. The male/female ratio was 1.21, but the ratio decreased with increasing age. The duration of chest pain showed a continuous spectrum between angina and infarction, with a short duration of chest pain not being useful for excluding the diagnosis of myocardial infarction. Hypertension was more common than hypercholesterolemia in this study, although the prevalence of the latter increased slightly with time, along with the shift towards a modernized occupational pattern. Smoking was a more important risk factor for ischemic heart disease in younger individuals than in the elderly, and diabetes mellitus was highly associated with the development of myocardial infarction. The incidence of radiologically diagnosed cardiac hypertrophy and aortic calcification decreased over time. These changes may have resulted in part from improved blood pressure control and the development of new antihypertensive and cholesterol-lowering agents. (Jpn Circ J 1998; 62: 675 - 679)

The risk of thromboembolism after cardioversion of atrial flutter is controversial. The present study provides evidence for blood stasis in the atria of patients with atrial flutter and for gradual recovery of atrial contraction after cardioversion, which justifies prophylactic treatment at cardioversion, as for atrial fibrillation. We examined atrial thrombi and peak flow velocity in the left atrial appendage as an index of blood stasis in 5 consecutive patients with atrial flutter. Transesophageal echocardiography revealed a thrombus in 1 patient, and peak flow velocity in the left atrial appendage was inversely correlated with left atrial dimension (r=-0.90, p

Abstract We examined whether shear stress can inhibit vascular smooth muscle cell (VSMC) proliferation in vitro directly. Human VSMCs were exposed to fluid flow for 24 hours using a cone-plate apparatus, and their proliferation was inhibited significantly by shear stresses of 1.4 and 2.8 Pa (14 and 28 dyne/cm 2 ), according to the magnitude. Next, we investigated whether transforming growth factor-β1 (TGFβ1), which is known to be an important cytokine that suppresses VSMC proliferation, is the predominant mediator of shear-induced inhibition of VSMC growth. After exposure of VSMCs to shear stress (2.8 Pa) for 24 hours, gene expression of TGFβ1 and, interestingly, tissue-type plasminogen activator, which converts plasminogen to plasmin, an activator of TGFβ1, increased twofold and fivefold, respectively. The levels of both latent and active forms of TGFβ1 in conditioned media of VSMCs exposed to fluid flow increased significantly. An anti-TGFβ1 antibody reversed shear-induced inhibition of VSMC growth significantly. We concluded that shear stress inhibited VSMC proliferation in vitro and this inhibition was mediated predominantly by TGFβ1 in an autocrine manner. These data suggest that shear stress plays an important role as an inhibitor of atherogenesis in endothelium-desquamated lesions.

Some patients with acute myocardial infarction (AMI) develop further ST elevation at reperfusion by percutaneous transluminal coronary angioplasty (PTCA). This study reports the ST deviation at reperfusion by direct PTCA in relation to the clinical factors and the recovery of left ventricular (LV) systolic function. Fifty-two patients with anterior wall AMI were treated with direct PTCA. They were classified into the following 3 groups according to the change in ST elevation at reperfusion: increase of ≥20% (ST reelevation); reduction of ≥20% (ST resolution); and the other (ST no change). Angina pectoris preceding AMI occurred less often in the ST reelevation group (ST reelevation group, 38%; ST no change group, 81%; ST resolution group, 70%; p < 0.05). Recovery of LV ejection fraction during the first month after direct PTCA was significantly poor in the ST reelevation group in contrast to the ST resolution group (ST reelevation group, −6.3 ± 13%; ST no change group, 18 ± 20%; ST resolution group, 45 ± 29%; p < 0.0001). The change in ST elevation at reperfusion was an index predicting the recovery of LV systolic function in the reperfusion by direct PTCA. Some patients with acute myocardial infarction develop further ST elevation at reperfusion by percutaneous transluminal coronary angioplasty. It is an index predicting the poor recovery of left ventricular systolic function in the chronic phase.

The cardiac electrophysiologic effects of parathyroid hormone (PTH) were studied in three different experimental models. Purified synthetic human parathyroid hormone (hPTH 1-84), at a dose of 30 ng/g body weight (BW), prolonged the QT interval of surface ECGs in intact guinea pigs. To further clarify the mechanisms of the QT prolongation caused by hPTH, the action potentials of guinea pig papillary muscle were recorded by conventional microelectrode techniques. hPTH (10(-7)M) prolonged the action potential duration without changing the action potential amplitude, resting potential, maximal upstroke velocity of the action potential, or maximal repolarization rate. hPTH affected only the plateau phase, in a concentration-dependent fashion. The half-maximum concentration was 6.8 x 10(-8)M for action potential duration at 30% repolarization (APD30), 3.2 x 10(-8)M for APD50, and 2.1 x 10(-8)M for APD90. In isolated single guinea pig ventricular cells, the patch clamp method was used to record the slow inward calcium current (ICa) and delayed rectifier potassium current (IK) responsible for the action potential plateau phase. hPTH increased the peak amplitude of ICa at + 10mV by an average of 42%, and increased IK at + 10mV by 85%. These results indicate that, in ventricular muscle, hPTH prolongs the action potential duration and QT interval by the balance of the prolongation effect on APD by enhancing the slow inward calcium current and the shortening effect on APD by enhancing the delayed rectifier potassium current.

To develop a noninvasive method for evaluating the influence of aortic wave reflection on left ventricular ejection, the carotid pulse wave and the pulsed Doppler wave in the left ventricular outflow tract were evaluated in 35 patients. Agreement between the pulsed Doppler waveform and the aortic flow velocity contour (obtained invasively) was verified by Fourier analysis. The carotid augmentation index was used to determine the magnitude of the aortic pressure wave reflection. A Doppler index named “DR1/3” was defined as the ratio of deceleration at the first one-third in the deceleration phase to the peak flow velocity of the pulsed Doppler. This index was validated by close correlation with the carotid augmentation index (n = 48,r = 0.70,P < 0.01). Both nitrates and nifedipine induced a significant decrease in DR1/3 (indicating an increase in left ventricular ejection flow) in relation to a reduction of the reflected pressure wave. The new noninvasive index, DR1/3, is useful in evaluating the influence of aortic wave reflection as part of the left ventricular afterload and in assessing the benefit of treatment aimed at reducing wave reflection.

The Watanabe Heritable Hyperlipidemic (WHHL) rabbit is a widely studied animal model for the human genetic disorder familial hypercholesterolemia, and spontaneously develops atherosclerotic disease. We studied the growth characteristics of cultured vascular smooth muscle cells (VSMC) from WHHL rabbits compared with VSMC from Japanese white rabbits. We measured cell proliferation, DNA synthesis, and c-myc proto-oncogene expression, in response to growth stimuli such as fetal bovine serum (FBS) and platelet-derived growth factor (PDGF). VSMC from Japanese white rabbits exhibited a 4-fold increase in cell numbers during a 5-day incubation period compared with those from WHHL rabbits. FBS and PDGF stimulated DNA synthesis, as measured by thymidine incorporation into VSMC, in both Japanese white rabbits and WHHL rabbits, however the response was significantly higher in the former strain. The intracellular pH value of VSMC determined using the pH-sensitive fluorescence dye 2′,7′-bis-carboxyethyl-carboxyfluorescein was significantly higher in WHHL rabbits than in Japanese white rabbits. Proto-oncogene c-myc was induced by exposure of VSMC to FBS, however there was no significant difference in c-myc mRNA levels between the two strains. These results suggest that VSMC from WHHL rabbits are not genetically growth accelerated, but show decreased growth response to growth stimuli.

Complete atrioventricular block (CAVB) during cardiac catheterization is a rare complication. We describe a patient with preexisting complete right bundle branch block who developed CAVB during left-sided cardiac catheterization. CAVB was induced when a left-sided catheter was passed through the aortic valve. We speculate that the patient's His bundle was injured by mechanical compression. Physicians should always pay attention to the possibility of the development of CAVB during cardiac catheterization, particularly in patients with preexisting heart block.

We have investigated the growth characteristics of adult rat ventricular cells (ARVC) in culture from 8-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Protein synthesis in ARVC estimated from tritiated leucine uptake was augmented in both strains after exposure of cells to either norepinephrine or fetal bovine serum (FBS), but the response was significantly smaller in SHR than in WKY. A relative increase in the protein content of ARVC incubated with norepinephrine or FBS was also smaller in SHR than in WKY. These results demonstrate that SHR cardiac myocytes are not genetically growth-accelerated and show a decreased growth response to growth stimuli such as norepinephrine and serum during the adult period.

Nifedipine 10 mg, administered sublingually to 12 patients following diagnostic cardiac catheterization, caused reduction in systemic resistance, and change of impedance together with alteration in contour of the ascending aortic and left ventricular pressure waves. The substantial reduction in ascending aortic and left ventricular systolic pressure with nifedipine occurred despite an increase in stroke volume and cardiac output, and was associated with similar reductions in mean pressure and indices of wave reflection. In the same patients, there were no significant changes in pulmonary vascular resistance or impedance, nor in pulmonary artery or right ventricular pressure pulse contour. For the systemic circulation, as with nitroglycerin and nitroprusside, reduction in wave reflection appears to be an important factor in the drug's action and for its beneficial effects on cardiac load in the treatment of angina pectoris, systemic hypertension and left ventricular failure. Thus the observed effects of nifedipine were attributed to vasodilatation of the systemic arteries and arterioles.

Background and Purpose— We sought to establish the relation between the pulsatile components of pressure and flow waveforms in the carotid artery and their change with age. Methods— Distention (pressure) and axial flow velocity waveforms were recorded noninvasively and simultaneously from the common carotid artery of 56 healthy subjects aged 20 to 72 years. Results— There was a close relation between the time intervals of pressure and flow waves: from foot to first shoulder or peak, to second shoulder or peak, and to incisura ( r =0.97, P P Conclusions— Arterial stiffening with aging increases carotid flow augmentation and can explain the increasing flow fluctuations in cerebral blood vessels. Measurement of carotid FAI may provide a gauge for risk of cerebral microvascular damage, just as PAI provides a gauge for risk of left ventricular hypertrophy and failure.

A 66-year old woman had had intermittent anterior chest pain and upper abdominal pain for 15 years. Angina pectoris was diagnosed at the age of 51 years, as she had typical anginal pain that was relieved by nitroglycerine, although coronary arteriography was normal and the ergonovine provocative test was negative. She had undergone cholecystectomy at the age of 38 years. Her bile duct pressure increased markedly after morphine injection and severe pain with the aforementioned distribution was produced. Postcholecystectomy syndrome due to sphincter of Oddi spasm was diagnosed and her pain was relieved by endoscopic sphincterotomy.

A case of marked reduction of the bezafibrate-induced increase of high-density lipoprotein (HDL)-cholesterol by low-density lipoprotein apheresis (LDL-apheresis) has not been previously reported.A 68-year-old Japanese man with arteriosclerosis obliterans (ASO), diabetes mellitus, and hyperlipidemia underwent LDL-apheresis, followed by the concomitant bezafibrate administration. Plasma lipids of pre- and post-LDL-apheresis were measured and apolipoprotein E (apoE) localization of the pre- and post-LDL-apheresis was detected by agarose gel electrophoresis.Plasma concentrations of the total cholesterol, LDL-cholesterol, triglyceride, and HDL-cholesterol of pre-LDL-apheresis were 4.78 +/- 0.36, 2.74 +/- 0.24, 2.44 +/- 0.52, and 0.92 +/- 0.10 mmol/l, respectively; those of the post-LDL-apheresis were 1.94 +/- 0.31, 0.72 +/- 0.13, 0.81 +/- 0.38, and 0.86 +/- 0.11 mmol/l, respectively. LDL-apheresis reduced HDL-cholesterol by 6.4% (p=0.346). During the bezafibrate administration, plasma concentrations of the above of pre-LDL-apheresis were 5.24 +/- 0.34, 3.28 +/- 0.22, 1.26 +/- 0.25, and 1.39 +/- 0.21 mmol/l, respectively; those of the post-LDL-apheresis were 2.25 +/- 0.44, 0.80 +/- 0.12, 0.58 +/- 0.19, and 1.18 +/- 0.16 mmol/l, respectively. LDL-apheresis reduced HDL-cholesterol by 15.2% (p0.01). Plasma apolipoprotein E detected between the prebeta- and alpha-mobility was markedly lower after the LDL-apheresis in the agarose gel electrophoresis.The removal of the bezafibrate induced an increase of the HDL-cholesterol by LDL-apheresis.

Two thousand, seven hundred and thirty-three patients with acute myocardial infarction (AMI) who were admitted to our 11 institutions between 1983 and 1988, examined by coronary arteriography and discharged alive, were followed for an average of 2.9 years. During the follow-up period, 212 patients (7.6%) died. The factors that governed the prognosis of myocardial infarction after discharge were advanced age, female gender, obesity, previous infarction, angina pectoris more than 1 month before the onset of AMI, post-infarction angina, multiple-vessel diseases, advanced stage by Killip's and/or Forrester's classification on admission, elevated pulmonary capillary arterial pressure, decreased cardiac index, decreased left ventricular ejection fraction, increased left ventricular end-diastolic volume and left ventricular aneurysm before hospital discharge. Patients with ventricular tachycardia or ventricular fibrillation during hospitalization showed a poor prognosis. In contrast, patients who received intracoronary thrombolysis, or emergent and/or elective percutaneous transluminal coronary angioplasty showed a favorable prognosis.

The subjects consisted of 2,733 patients with acute myocardial infarction (AMI) who were admitted to our 11 institutions between 1983 and 1988, examined by coronary arteriography, and discharged alive. The patients were followed for an average of 2.9 years after discharge. During the follow-up period, re-infarction occurred in 172 patients (6.3%). The factors associated with re-infarction were total cholesterol of more than 250 mg/dl, HDL-cholesterol of less than 35 mg/dl and diabetes mellitus. The rate of re-infarction was also high in patients who had had a previous infarction before admission, angina pectoris before or after the onset of AMI or multiple-vessel disease. In contrast, intracoronary thrombolysis reduced the rate of re-infarction.

Psychological and social factors can profoundly influence a patient's success in adhering to a prescribed self-care regimen. A total of 34 inpatients with type II diabetes who attended the diabetes education program at a single clinic were studied as a retrospective cohort, beginning between 6 and 12 months after discharge. At the start of the study, the patients were classified into two groups, those with good control and those with poor control of diabetes, based on the rate of change of the glycosylated hemoglobin (HbAlc) value relative to the value at admission. Data for each patient were collected retrospectively from their medical records. Patients' family function was assessed by the adaptability, partnership, growth, affection, and resolve (APGAR) scoring system. Multiple regression analysis was used to determine the effect of demographic, medical, and social factors on metabolic improvement. The family APGAR score was higher in the good control group than in the group with poor control.(Internal Medicine 32: 763-767, 1993)

This study was designed to evaluate left coronary vascular bed reserve in hypertensive cardiac hypertrophy. The subjects were eight patients with hypertensive cardiac hypertrophy (HT) and nine patients with normal coronary flow (N). Coronary sinus flow (CSF) was measured by a continuous thermodilution method, and the ascorbic acid-platinum reaction was employed for the mean transit time measurement (T0-T2) of left coronary flow. T0 is ascorbic acid injection into the left coronary orifice and T2 is the maximal point of detecting ascorbic acid volume in the coronary sinus. Volumes for the coronary vascular bed (CVB) were obtained by multiplying CSF and T0-T2. CVB value in the HT patients was more than that in the control group at control heart rate, but was less than in N at a high pacing rate. CSF in the HT patients was more than that in the N group at any heart rate, and the CVB values per unit of myocardial mass were less in the HT patients than in the N group. The pressure rate product in the HT patients was more than that in the normal coronary flow group. The transit time of left coronary flow in the HT patients was less than that in the N group. The CVB in the HT group was more than that in the normal coronary group at control heart rate and less than that in the normal group at a high pacing rate. Cardiac work in the HT patient was thus shown to be greater than that in the normal group.

A 53-year-old male was admitted to the hospital because of Candida albicans endocarditis. He had had a thoracoplasty due to pulmonary tuberculosis and showed severe restructive lung function. In 1987 and '89, trachiostomy was made because of respiratory failure. The patient was well until nine months earlier, when he consulted a physician because of fever. The investigations failed in finding the cause of the fever. He was administered antituberculosis agents and antiinflammatory drugs but had a fever every day. Two months before admission, a cardiac ultrasonographic study showed evident vegetations with mitral regurgitation. From the above course and examinations, a diagnosis of Candida albicans endocarditis was made. Infusions of CEZ, TOB, PIPC and miconazole for more than one month was ineffective. In November, 1990, he was referred to our medical center for the purpose of operation. A blood culture proved Candida albicans infection. An intravenous administration of fluconazole 400 mg/day was begun. However, there was pulmonary bleeding probably due to heparin used for prevention of atrial thrombosis and he developed fever, hypoexemia, ventricular tachycardia, and hyponatremia. He underwent mitral-valve replacement with a SJM valve. Culture of the vegetated mitral valve again proved Candida albicans. After operation, hypoexemia, ventricular tachycardia, hyponatremia were improved gradually. However he had an eosinophilia, eruption, and dyspnea. We suspected a drug eruption of fluconazole. Lymphocyte stimulating test of fluconazole proved positive. After the episode, he had no symptoms and was discharged.

To determine the genesis of the high incidence of stenotic lesions of the left anterior descending artery (LAD) in the young, we have investigated the anatomical characteristics of coronary arteries in the following 3 groups; young (less than or equal to 40 yr) myocardial infarction (MI) patients with LAD lesions, young (less than or equal to 40 yr) patients without coronary stenosis and aged (greater than or equal to 60 yr) MI patients. The angle between the left main coronary artery (LMT) and the LAD in the young MI patient group (146.7 +/- 7.4 degrees) was significantly wider than those of the young normal (126.0 +/- 13.4 degrees) or the aged MI patient groups (127.1 +/- 18.6 degrees) (p less than 0.01, p less than 0.02, respectively). The angle between the LMT and the left circumflex artery (LCX), and the angle between the LAD and the LCX were not significantly different among the 3 groups. The LMT length in the young MI patient group was 18.3 +/- 4.7 mm, which was not significantly longer than those of the young normal (12.7 +/- 6.9 mm) or the aged patient groups (14.8 +/- 6.0 mm). The internal diameter ratio of the LAD and LCX was also not significantly different among the 3 groups. These results suggest that the angle between the LMT and LAD was significantly wider in young MI patients, and should be regarded as an inherited characteristic influencing the development of coronary atherosclerosis of the LAD, particularly in young MI patients.

To explore the role of calcium channels in hypertension, dihydropyridine ([3H]PN200-110) binding to heart, brain, and skeletal muscle microsomes of 4-, 8- and 15-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats was measured. At a constant Ca2+ ion concentration (pCa 3.0), maximal binding (Bmax) of dihydropyridine binding to heart and brain microsomes was significantly enhanced in 8- and 15-week-old SHR compared with WKY rats (p less than 0.01), whereas this phenomenon was not observed in 4-week-old SHR and WKY rats. Bmax and dissociation constant (Kd) values for skeletal muscle microsomes from SHR showed no difference compared with WKY rats irrespective of age. Dihydropyridine binding to heart microsomes, brain microsomes, and solubilized skeletal muscle microsomes exhibited strong calcium dependence. The Ca2(+)-dependent dihydropyridine binding curves for heart showed a Hill slope, and pK 0.5 values for 15-week-old SHR and WKY rats were 0.70 +/- 0.12 and 4.66 +/- 0.12 versus 0.72 +/- 0.12 and 5.66 +/- 0.08 (n = 4, mean +/- SD), respectively, indicating that 15-week-old SHR require 10-fold higher calcium concentration than WKY rats to promote dihydropyridine binding. The pK 0.5 values of calcium for brain and solubilized skeletal muscle calcium channels in 15-week-old SHR were also significantly lower than in WKY rats. This difference first became apparent in SHR and WKY rats as early as 4 and 8 weeks after birth. These results suggest that enhancement of calcium channel density might occur in the heart and brain of SHR in response to elevated blood pressure and that reduced calcium sensitivity of dihydropyridine binding to calcium channels might be a primary characteristic of this rat strain.

We have investigated the effect of interleukin-1 (IL-1) on the growth of vascular smooth muscle cells (VSMC) isolated from rat aortae. Murine recombinant IL-la increased tritiated leucine incorporation into VSMC. IL-1 also stimulated tritiated thymidine uptake by VSMC in a dose-dependent manner. On the other hand, Ca 2+ -channel blocker, verapamil, inhibited the IL-1-induced thymidine uptake by VSMC with an IC 50 of 10 −8 M. Antibody specific for platelet-derived growth factor (PDGF) also totally inhibited the IL-1-induced thymidine uptake. IL-1 showed no effects on the intracellular CaZ+ level in VSMC. Above results support the premise that IL-1 promotes the growth of VSMC via induction of endogenous PDGF production and might thus participate in the abnormal proliferation of VSMC that occurs early in atherogenesis.

We investigated, by case-control study, the relevance of psychosocial factors on the prevalence of acute ischemic heart disease (IHD) in middle aged Japanese men. We questioned 109 acute IHD patients and 80 individuals in an age-adjusted sampled control group. Multiple logistic regression analysis showed the following statistically significant factors: hypertension (odds ratio 4.01, p less than 0.001), Type A behavior pattern (2.25, p less than 0.05) and high job demand (2.23, p less than 0.02). No direct influence of family function or social support to the prevalence of acute IHD was apparent. These results suggest that, among men in Japan, Type A behavior pattern and high job demand represent psychosocial risk factors of IHD. Due to the case-control protocol, causal relationships cannot be decided. The limitation of the study design is discussed within that context.

The effects of age on the interrelation between the physical properties of the arterial tree (aortic input impedance) and left ventricular performance (cardiac output) were studied in 45 subjects, aged 19 to 62 years, without apparent cardiovascular disease. Ascending aortic pulsatile pressure and blood flow velocity were measured with a multisensor catheter and cardiac output by green dye or the Fick method. Heart rate and end-diastolic aortic pressure remained unchanged with age, whereas aortic systolic, mean and pulse pressures and aortic radius increased. In subjects younger than 30 years, early systolic pressure usually exceeded late systolic pressure (type C beat); in subjects older than 50 years, late systolic pressure usually exceeded early systolic pressure (type A beat). In 55% of subjects aged 30 to 50 years, early and late systolic pressures were essentially equal (type B beat). The impedance spectra from all subjects showed fluctuations about the characteristic impedance (index of elastance) that were greater in the older subjects. Peripheral resistance increased 37% (r = 0.47, p less than 0.001) over the age range of 20 to 60 years, whereas characteristic impedance increased 137% (r = 0.66, p less than 0.001). The fundamental impedance modulus increased, and the impedance modulus minimum shifted to a higher frequency. These changes in the impedance spectral pattern indicate that the ascending aorta becomes stiffer and the cross section of the peripheral vascular bed decreases with age, causing increased pulse wave velocity and wave reflection.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of sublingual glyceryl trinitrate (GTN) were studied in ten patients without heart failure during diagnostic cardiac catheterisation following angiography. GTN caused substantial reduction in peak left ventricular and aortic pressure (19 mmHg) with lesser reduction in mean aortic pressure (9 mmHg) and no change in diastolic aortic pressure. Reduction in stroke volume (by 15%), associated with fall in left ventricular end diastolic pressure (by 4 mmHg) was insufficient to explain the marked (17 mmHg - 34%) reduction in pulse pressure. Decrease in pulse pressure was associated with loss of the late systolic peak on both the aortic and left ventricular pressure wave. This peak is caused by pulse wave reflection. GTN caused no change in peripheral resistance or in indices of aortic compliance (characteristic impedance, total arterial compliance) but was associated with reduction in fluctuations of both modulus and phase of aortic impedance. All these changes in pressure waves and in impedance spectra are explicable on the basis of decreased peripheral wave reflection. This can be attributed to the known vasodilatory effect of GTN on the peripheral arteries. Simulation of arterial vasodilatation in a multi-branched model of the systemic arterial system confirmed this interpretation. Dilatation of peripheral arteries explains in part the beneficial effects of GTN in adult man.

In forty-one patients with various heart diseases including 29 with LVH, the vectorcardiograms of Frank system and angiocardiographic findings correlated minutely. Based on the left ventricular wall thickness in end-diastole, left ventricular end-diastolic volume, and the length of the long axis of the left ventricle obtained in angiocardiograms, typical left ventricular hypertrophy was classified into types 1a, 1b, 2a, 2b anatomically. The vectorcardiograms in these 4 types represented different patterns with regard to the QRS and T loops respectively. The QRS voltage in the left ventricular hypertrophy closely correlated to the left ventricular wall thickness in end-diastole, the left ventricular end-diastolic volume, and the left ventricular mass. Marked ST and T changes in the left ventricular concentric hypertrophy characterized by increase in wall thickness without definite chamber enlargement may be closely related to the abnormal muscle state with the increased left ventricular wall thickness, the probably due to relative hypoxia in origin. The Q loop of patients with severe left ventricular concentric hypertrophy was definitely differentiated from that of most patients with the pure left ventricular eccentric hypertrophy which was characterized by chamber enlargement with usually slight thickening of the wall. A possible mechanism regarding inconspicuous or prominent Q loops in both concentric and eccentric LVH was presented. An important factor of the delay of the time of occurrence of the spatial R vector in the left ventricular eccentric hypertrophy is the greater distance of the intraventricular conducting pathways caused by the left ventricular dilatation. By means of assessing the vectorcardiogram of the left ventricular hypertrophy, relatively exact anatomy of the left ventricular hypertrophy can be determined.

In forty-five patients with various heart diseases, geometric changes and time course of wall stress were studied by the use of angiographic technique. 1) Relative wall thickness in diastole was signiflcantly decreased in mitral insufficiency. 2) Ejected fraction was reduced in the cases with ventricular hypertrophy inappropriate to dilatation. 3) Ejected fraction was reduced in the subjects where stress at end-ejection was higher than at the onset of ejection. 4) In left ventricular failure the duration of peak stress was longer and time to peak stress was prolonged . 5) After digitalization, peak stress was lowered and time to peak stress was shortened. 6) To analyze the myocardial contractile state, the time course of wall stress during con-traction can be one of the essential factors, and the systolic ejected fraction might be considered an expression of myocardial condition.

In this paper, the correlation between the maximal QRS vector or the mean electrical axis by Frank lead system and the maximal long axis or the half area long axis of the left ventricle obtained by biplane angiocardiogram in the frontal and left sagittal planes in thirty patients with various heart diseases were studied. Cases with marked ventricular hypertrophy or abnormalities in the intraventricular conducting pathways were excluded as much as possible. Compared to contemporary studies the approach utilized by the present authors appears to be more favorable, viz; (1) the mean electrical axis was calculated from the corrected orthogonal lead system, (2) the anatomical position of the left ventricle was measured exactly and minutely from the angiocardiogram in the frontal and left sagittal planes, and (3) the end-diastolic volume and the wall thickness of the left ventricle were determined from the left ventriculogram in order to assess the grade of left ventricular hypertrophy, while pressure measurements in the right heart chambers detected right ventricular hypertrophy.

The left ventricular myocardial function in the ejection phase of auxotonic contraction was investigated in direct relation to aortic distensibility in twenty-five patients with varying heart lesions. Analysis of the aortic pressure curve and the ascending aorta volume obtained by routine left heart catheterization and biplane angiocardiography provided an approach to compute aortic distensibility. The mean value of the aortic distensibility in all patients was 0.847 ± 0.430 S.D. percent per mmHg pulse pressure. In patients with normal left ventricular (LV) function, the aortic distensibility demonstrated a significant inverse relationship to the duration of the LV wall stress at top 20 percentile of its peak (r=-0.71), and also a positive one to the contractile element velocity at the peak stress (r=0.70). Patients with LV dysfunction defined by ejection fraction of below 50% showed an increase in duration of higher stress with relatively low aortic distensibility. This characteristic feature of the aortic property and stress-time relation in the ejection phase observed in LV dysfunction were not always found to concur with low maximal contractile element velocity (Vmax) which was computed in the isovolumic phase. These results suggest that the aortic distensibility is one of the major determinants on LV myocardial force and velocity development, and that evaluation of myocardial functions in the ejection phase should be made as well as in the isovolumic phase.

The perfusion territories in polar representations of stress Tl-201 rotational myocardial imaging in patients with angina pectoris who had one diseased coronary segment were analyzed. The lesions proximal or distal to the first major septal perforator in left anterior descending arteries were detected by the presence or absence of defects at the base of the anterior septum. Right coronary artery lesions were detected by the presence of defects at the basal posterior septum, in contrast to the preservation of myocardial uptake at this portion in lesions of the left circumflex artery. The specific defect patterns were detected in cases with lesions at the first diagonal, obtuse marginal, and posterolateral branches. Recognition of these defects in the polar maps allows detailed detection of diseased coronary arterial branches.

An elderly woman with Lutembacher's syndrome remained asymptomatic until the age of 55, when she was treated for exertional dyspnea with digitalis and diuretics. She died of gastrointestinal hemorrhage and hepatic failure at the age of 69. The autopsy revealed a large atrial septal defect and mitral stenosis without rheumatic changes. This patient is the oldest reported survivor of Lutembacher's syndrome with nonrheumatic mitral stenosis.

To evaluate whether a significant statistical correlation exists between earlobe crease (EC) and coronary heart disease (CHD), 1000 Japanese adult patients (573 males, 427 females) were examined for the presence or absence of EC, clinical or angiographic evidence of CHD, and the following coronary risk factors: male sex, age over 50 years, obesity, hypertension, diabetes mellitus, cigarette smoking, and hyperlipidemia. Patients were divided into two groups according to clinical evidence of CHD: 237 patients with angina pectoris and/or myocardial infarction (CHD+ group); 720 patients without evidence of CHD (CHD- group). Coronary angiography was performed on 200 patients from this sample population; these patients were also divided into two groups: 119 patients with greater than 50% luminal narrowing of at least one major coronary artery (stenosis+ group); 81 patients with no significant atherosclerotic changes in the coronary arteries (stenosis- group). EC was present in 58 of 237 CHD+ patients (24.5%) but in only 35 of 720 CHD- patients (4.8%; P less than 0.001); it was present in 31 of 199 stenosis+ patients (26.1%) but in only 3 of 81 stenosis- patients (3.7%; P less than 0.01). EC was also found to correlate significantly with some coronary risk factors; the correlations between the presence of EC and the presence of CHD and coronary risk factors were investigated by multivariate analysis. In a multivariate setting, the existence of CHD and an age of over 50 years was significantly related to the presence of EC. To investigate the relationship between EC and advancing age, all patients were separated into age-groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The prognostic values of indices obtained by M-mode and two-dimensional echocardiography (Echo) and by cardiac catheterization (Cathe) were assessed in patients with idiopathic dilated cardiomyopathy. Fifty-one patients with this disorder (38 males and 13 females) were studied for an average of 4.2 years. Of those, 24 died of cardiac causes during follow-up. The overall 5-year survival rate was 49%. Significant differences between the surviving patients and the patients who died were noted in the following indices measured by Cathe: left ventricular end-diastolic volume (LVEDV), left ventricular end-diastolic pressure (LVEDP), ejection fraction (EF), and the cardiac index (CI). The 5-year survival rate in patients with the following index values measured by Cathe at the initial examination were: LVEDV ≥ 150 ml/M2 - 29%; LVEDP > 12 mmHg - 35%, EF < 30% - 21%, and CI < 3.0 L/min/M2 - 29%. In contrast, the 5-year survival rate in patients with the following parameter values measured by Echo were: left ventricular end-diastolic dimension ≥ 45 mm/M2 - 16%; left atrial dimension ≥ 25 mm/M2 - 12%; ejection fraction < 30% - 31%; and a relative wall thickness (a ratio of left ventricular posterior wall thickness to left ventricular end-diastolic dimension) ≤ 0.12 - 9%. In assessing the cumulative survival rate, the indices provided by Echo revealed similar values when compared with those obtained by Cathe. The relative wall thickness determined by Echo would be the most reliable parameter for forecasting the 5-year survival rate. In the majority of patients (22/24) who died during the observation period, the relative wall thickness gradually decreased to less than 0.12. Therefore, a relative wall thickness below 0.12 would be the most reliable index for detecting a poor prognosis case. It is concluded that echocardiographic observation of patients with idiopathic dilated cardiomyopathy can provide information useful not only in prognosis but also in assessing the effect of medical treatment.

Implication of aortic input impedance and left ventricular coupling were investigated in three series of studies. In a clinical study, the ascending aortic flow velocity and pressure were simultaneously recorded from a multisensor catheter, and input impedance was calculated from 8 harmonics of aortic pressure and flow. Left ventricular wall stress was calculated from diameters and wall thickness of cineventriculogram and simultaneous recording of left ventricular pressure. In the experimental study, programmable artificial pulsatile pump was used to control pulsatile blood flow in dogs. The pressure-flow relationship in the arterial system had slightly convex curves toward the pressure axis with a critical turning pressure, so the arterial system had low output--high resistance and high output--low resistance characteristics. Therefore, the failed heart should inevitably eject the blood against stiffened vascular beds. Increased work load of the ventricle as expressed by sustained ventricular wall stress was determined mainly by the exaggerated late systolic pressure due to increased input resistance and increased low frequency pulsatile component of the input impedance. These findings are especially important for relieving additional work load of the ischemic heart, which have higher pressure wave reflection.

To clarify the mechanical adaptation and interference of coronary vessels, we studied hemodynamics of coronary circulation in control and 4 different pacing rates (80, 100, 120, 150/min) in 5 patients with angina pectoris (AP) and in 5 patients with hypertrophic cardiomyopathy (HCM). Coronary sinus flow (CSF) was measured by a Webster's thermodilution catheter, and we applied ascorbic acid-platinum reaction for the mean transit time measurement in left coronary flow (t0-t2). Coronary vascular bed (CVB) was obtained by multiplying CSF and t0-t2. CSF in AP gradually increased from 104 +/- 21 ml/min at 72/min to 148 +/- 42 ml/min at 120/min, while CSF in HCM changed slightly from 91 +/- 25 ml/min at 64/min to 94 ml/min at 120/min. Average t0-t2 in HCM was 6.0 +/- 1.6 sec in control which was significantly lower than that in AP (7.8 +/- 0.7 sec). Calculated CVB in AP increased at any given heart rate up to 120/min (13.5 +/- 2.4, 15.8 +/- 1.7, 15.0 +/- 4.7, 15.1 +/- 4.3 ml), but CVB in HCM decreased from 9.1 +/- 2.3 ml at 64/min to 8.1 +/- 1.7 ml at 120/min. These data suggest that myocardial compression and suction at different heart rates and with different cardiac muscle structures play an important role for beat to beat adjustment of coronary circulation in cardiac cycle.

Seventy-four patients with unstable angina are reviewed. A rather high incidence (65%) of a changing pattern syndrome was observed in the study group. A history of prior myocardial infarction was obtained in 22 patients (30%). Fifty-seven patients (77%) were investigated using coronary angiography : 15 did not have any significant occlusive disease but are included in this study ; single vessel disease was present in 20, double in 8 and triple in 14. Ten patients (13.5%) had myocardial infarcts which had occurred between 48 hours and 3 months after admission, and no patients died during this period. Patients who on admission had resting angina of new onset were more likely to have a worse short-term prognosis. Four patients underwent coronary bypass surgery in the first year of the follow-up period because of unsuccessful medical treatment. Six patients died within the first 4 years. Of the 6 deaths, 5 had triple vessel disease and one did not have any significant coronary stenosis. Mortality rate at 2 years was 2.7% and at 4 years 10.3%. This low mortality is probably attributable to a low incidence of 2- or 3-vessel disease.

To understand the influence of the aging process on left ventricular/arterial coupling (or interaction), it is important first to consider the effects of age on ventricular and arterial functions separately. The function of the left ventricle is to pump blood (the cardiac output) through the systemic arterial system to the organs and tissues in an amount sufficient to meet their metabolic requirements. The arterial system has two distinct and separate functions: (1) It serves as a vascular conduit system that delivers blood at high pressure to the various peripheral beds and (2) it serves as a buffering system (Windkessel) that smooths out pulsations resulting from intermittent ventricular ejection so that the capillaries receive a steady or continuous flow of blood.

The antianginal effects of diltiazem and nifedipine alone and in combination were evaluated in a double-blind, randomized, placebo-controlled trial in 11 patients (nine men and two women, 57 +/- 8 years old) with stable effort angina. Each patient received placebo, 30 mg of diltiazem, 10 mg of nifedipine, and 30 mg of diltiazem plus 10 mg of nifedipine four times daily for 1 week each. Antianginal efficacy was assessed by means of a treadmill exercise test. The exercise tolerance time was significantly prolonged from 235.1 +/- 52 (placebo period) to 342.2 +/- 101 sec by diltiazem (p less than .01) and to 325.6 +/- 73 sec by nifedipine (p less than .01). The drug combination further prolonged exercise time to 451.1 +/- 103 sec, which was significantly longer than the interval attained with either diltiazem (p less than .01) or nifedipine (p less than .01) alone. The plasma concentration of diltiazem was unaffected by the addition of nifedipine, whereas the plasma nifedipine concentration was significantly increased from 34.8 +/- 11 to 106.4 +/- 37 ng/ml (p less than .001) by the concomitant administration of diltiazem. These data suggest that exercise tolerance in patients with effort angina is increased by the concomitant administration of diltiazem and nifedipine associated with an increase in the nifedipine plasma concentration.

Total left ventricular external power and aortic input impedance spectra were calculated from recordings of pulsatile pressure and flow in the ascending aorta of 22 human subjects undergoing cardiac catheterization. Eleven subjects had increased aortic pressure (systolic 153 +/- 3.8[SEM] mm Hg, p less than .001; diastolic 91 +/- 2.4 mm Hg, p less than .03; mean 118 +/- 2.4 mm Hg, p less than .001) and constituted the group with mild hypertension (average age 50 +/- 1.9 years). The other 11 (age-matched) subjects had normal arterial pressures and constituted the control group. Cardiac output in the hypertensive group was abnormally high (6.9 +/- 0.3 liters/min, p less than .04) compared with that in control subjects (6.1 +/- 0.2 liters/min), so that peripheral resistance was similar. Characteristic aortic impedance (index of aortic elastance) was increased in the hypertensive group (142 +/- 19 vs 72 +/- 4.5 dyne-sec-cm-5, p less than .002), as was the fluctuation of impedance moduli and phase. These elevated pulsatile components of arterial load were associated with a significant (p less than .002) increase in pulsatile left ventricular external power (89%), and the increased cardiac output was associated with a significant (p less than .001) increase in steady flow power (31%). The ratio of pulsatile to total power was also increased (38%) in the hypertensive group (p less than .001). Increased characteristic aortic impedance in the hypertensive group suggests that the human aorta is stiffer, and fluctuations in the impedance spectra suggest increased or less dispersed wave reflections.(ABSTRACT TRUNCATED AT 250 WORDS)

1. Ciraulo DA: Mitral value fluttering. An ecbocardiographic feature of left atria1 myxoma. Chest 7’695, 1979. 2. Bourdillon PDV, Monro JL$ Johnson AM: Left atria1 myxoma with aortic regurgitation. Br Heart J 40575, 1978. 3. Clark RD: Case studies m echocardiograpby. A diagnostic workbook. Philadelphia, 1977, W. B. Saunders Co, pp 76. 4. Rose MR, Fox AC, Glassman E, Reed GE: Left atria1 myxoma and aortic regnrgitation Case report. J Thorac Cardiovasc Surg 66:797, 1974.

The development and reversal of tolerance to the hemodynamic and anti-anginal effects of isosorbide dinitrate in a sustained release form (ISDN-SR) were investigated in 11 male patients (mean age 58.9 y.o.) with stable effort angina. Treadmill exercise test, evaluation of hemodynamic parameters and measurement of plasma ISDN concentrations were performed during the control period, on the 1st, 7th and 14th days of therapy with 40 mg of ISDN-SR orally every 8 h and, subsequently, on the day when ISDN-SR was re-administered after a 72 h placebo period (17th day). Initially, exercise tolerance time (ETT) was prolonged significantly (p less than 0.001) by ISDN-SR from 257 +/- 50 sec in the control period to 434 +/- 55 sec on day 1. This prolongation was significantly reduced with sustained therapy and ETT was shortened to 332 +/- 69 sec on the 7th day (p less than 0.01 vs day 1) and 326 +/- 73 sec on the 14th day (p less than 0.01 vs day 1). The effects of ISDN-SR initially observed were restored after a 72 h placebo period and ETT was prolonged to 432 +/- 57 sec on the 17th day. The resting heart rate was increased significantly (p less than 0.01 vs control) and systolic blood pressure was decreased (p less than 0.001 vs control) by ISDN-SR on day 1. These changes were also diminished significantly (p less than 0.01 vs day 1) with sustained therapy and were restored after a 72 h nitrate-free interval.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this paper is to consider “ideal” ventricular/vascular coupling, and how this may be manifest in the time domain and in the frequency domain. The paper will also consider how such “ideal” coupling is achieved, and how it might be disturbed. The arterial system plays a crucial role in ventricular/vascular coupling since it separates the smallest vessels where flow is almost perfectly continuous from the ventricle, whose output is intermittent. Ventricular/vascular coupling can be assessed from measurements of pressure and flow in the ascending aorta (AA) (for left ventricle/systemic circulation), and in the main, pulmonary artery (MPA) (for right ventricle/pulmonary circulation). Ideal coupling is manifest as low pressure fluctuation in AA and MPA. Low pressure fluctuation results in pressure during systole being only slightly greater than pressure throughout the whole cardiac cycle, and pressure during diastole being only slightly less. This is desirable because pressure during systole determines ventricular output (when inotropic state and ventricular filling are constant), and ventricular metabolic requirement, while pressure during diastole in AA is a major determinant of coronary blood flow. In the frequency domain, “ideal” coupling is manifest as a correspondence between minimal values of impedance modulus in AA and MPA with maximal values of flow harmonics in AA and MPA, respectively. Factors responsible for “ideal” coupling have been identified as high distensibility of proximal arteries (with decreasing distensibility in peripheral arteries), wave reflection at arterial terminations, and a “match” between heart rate on the one hand and arterial length and wave velocity on the orther. This favourable “match” results in the heart operating for both systemic and pulmonary circulations close to a node of pressure and antinode of flow; this match is improved under conditions which simulate flight and fight. While ventricular/vascular coupling appears to be close to ideal in most large mammals, it appears to be less than ideal in adult humans and some small mammals including guinea pigs, rats, and mice. The cause for mismatch in small mammals is unclear. In humans however, finding are attributable to progressive arterial degeneration which is known to commence in childhood and is apparent in the elderly as dilated tortuous arteries, high pulse pressure, and high likelihood of developing ventricular failure.

In fourteen patients with aortic insufficiency, the interrelations among the systolic time intervals and other hemodynamic measurements were studied by means of cardiac catheterization and angiocardiography. The pre-ejection period was within the normal range in nine patients. The left ventricular ejection time and the total electromechanical systole were prolonged above normal in almost all the patients. The left ventricular ejection time corrected for heart rate exhibited a close inverse relationship to both the ejection fraction and the mean shortening velocity per unit length of the myocardium. These findings suggest that the left ventricular ejection time can be a non-invasive aid of clinical use in evaluating the left ventricular function in patients with aoric insufficiency.