Intramural Coronary Vessels Research Articles

Abstract 11198: Intra-Myocardial Dissecting Haematoma Presented as a Ventricular Tachycardia in a Patient With Remote Silent Myocardial Infarction

Intramyocardial dissecting haematoma (IMDH), a rare form of myocardial rupture, is recognised as a complication of acute myocardial infarction (MI) but can also occur as a result of a thoracic trauma or spontaneous rupture of intramural coronary vessels. Before the advent of advanced multi-modality cardiac imaging, IMDH was an autopsy diagnosis. In this report, we present a patient with recent onset of palpitation due to non-compromising ventricular tachycardia (VT). Post cardioversion ECG showed anterior-apical deep Q waves in keeping with prior silent MI. Transthoracic echocardiography showed severely reduced left ventricular ejection fraction due to extensive apical aneurysm and raised the possibility of protruding apical thrombus. Subsequent contrast echocardiography showed features compatible with extensive LV apical thrombus and raised the differential diagnosis of contained myocardial rupture and IMDH. During the two years follow-up guideline directed medical therapy for heart failure and antiarrhythmic medication stabilised patient at NYHA class I-II with no recurrence of VT. Multimodality imaging including cardiac CT and MRI confirmed the suspicion of IMDH. With this case we are highlighting the difficulties in the diagnosis and the controversies of the management of IMDH. Figure: A: ECG shows monomorphic VT. B: after chemical cardioversion, ECG shows sinus rhythm with old transmural extensive anterior MI. C: Transthoracic echocardiography, apical 4 chamber view shows aneurysmatic left ventricular apex with echo lucent space with mobile intraventricular membrane separating the true LV lumen and the dissecting hematoma (Asterix). D: Contrast enhanced echocardiography delineating the true LV cavity from the IMDH. E,F: Contrast enhanced CT showing the low attenuation hematoma located in the anterior LV apex. Note the calcification in the LV apical myocardium indication of prior transmural MI.

Virus-Negative Myopericarditis in Human Coronavirus Infection: Report From an Autopsy Series.

Virus-Negative Myopericarditis in Human Coronavirus Infection: Report From an Autopsy Series.

Effects of Testosterone Deficiency and Angiotensin II–Induced Hypertension on the Biomechanics of Intramural Coronary Arteries

BackgroundAndropause and hypertension also increase the risk of coronary artery damage. AimTo investigate the effect of testosterone deficiency and hypertension on intramural coronary vessels. Methods4 groups of 8-week-old Sprague-Dawley rats were studied: control male (Co, n=10), orchidectomized male (OCT, n=13), angiotensin (AII) hypertensive male (AII, n=10), and AII hypertensive and OCT (AII + OCT, n=8). Surgical orchidectomy was performed, and an osmotic minipump was inserted for chronic angiotensin II infusion (100 ng/min/kg). After 4 weeks, spontaneous tone and biomechanical properties of the intramural coronary resistance artery were investigated in vitro, by pressure microarteriography. OutcomesMorphology and biomechanics of the intramural coronaries were evaluated: the outer diameter, wall thickness–to–lumen diameter ratio, and tangential wall stress in the contracted and relaxed states. ResultsThe outer diameter was reduced in OCT and AII + OCT groups (on 50 mmHg 315 ± 20 Co; 237 ± 21 OCT; 291 ± 16 AII, and 166 ± 12 μm AII + OCT). The increased wall thickness–to–lumen diameter ratio resulted in lower tangential wall stress in AII + OCT rats (on 50 mmHg 19 ± 2 Co; 24 ± OCT; 26 ± 5 AII, and 9 ± 1 kPa AII + OCT). Spontaneous tone was increased in the hypertensive rats (AII and AII + OCT groups) (on 50 mmHg 7.7 ± 1.8 Co; 6.1 ± 1.4 OCT; 14.5 ± 3.0 AII, and 17.4 ± 4.1 % AII + OCT). Clinical ImplicationsAndropause alone can be considered as a cardiovascular risk factor that will further exacerbate vascular damage in hypertension. Strengths & LimitationsA limitation of our study is that it was performed on relatively young rats, and the conclusions might not apply to coronary remodelling in older animals with slower adaptation processes. ConclusionsTestosterone deficiency and hypertension damage the mechanical adaptation of the vessel wall additively: double noxa caused inward eutrophic remodeling and increased tone.Jósvai A, Török M, Mátrai M, et al. Effects of Testosterone Deficiency and Angiotensin II–Induced Hypertension on the Biomechanics of Intramural Coronary Arteries. J Sex Med 2020;17:2322–2330.

A rotating cerium anode X-ray system allows visualization of intramural coronary vessels after cardiac stem cell therapy for myocardial infarction.

Conventional angiography is insufficient for evaluating the therapeutic effect of cardiac regeneration therapy. A microangiographic X-ray system using a cerium anode was developed. Cerium has a characteristic X-ray with a peak at 34.6keV, which allows visualization of tiny amounts of iodine. The performance of the cerium anode X-ray system was evaluated in two excised normal canine hearts and in excised ischemic canine hearts treated with c-kit-positive cardiac stem cells (5 canines) or without cells (5 control canines). In the normal canines, branches penetrating from the left anterior descending artery into the myocardium were visualized, down to third-order branches. In just the treated hearts treated with stem cells, small vessels characterized by irregular vessel walls were observed. The cerium anode X-ray system allowed visualization of microvessels in excised ischemic canine hearts, and may evaluate the effect of cardiac stem cell therapy.

Allergic myocardial infarction

Allergic myocardial infarction

Parathyroid Carcinoma of the Mediastinum

Parathyroid carcinoma accounts for about 4% of all diseases of the parathyroid glands. It usually presents as a tumor mass in the neck region. Mediastinal parathyroid carcinoma has been reported very rarely. The present paper reports an ectopic parathyroid carcinoma in the anterior mediastinum in a 54-year male that failed to be recognized antemortem. The markedly elevated serum calcium levels were repeatedly put down to laboratory errors, and the clinical features of primary hyperparathyroidism were misjudged and managed only symptomatically. The terminal cardiogenic shock was associated with myocardial infarction. Coronary plastic surgery was carried out and a stent was placed. The postmortem examination found a solid elastic tumor mass (4 cm) firmly encapsulated in the upper half of the anterior mediastinum having trabecular structure, mild nuclear and cellular polymorphism, single irregular mitoses and an area of necrosis. The mass invaded the capsule and the surrounding adipose tissue, there were tumor emboli found in the lymph and blood vessels. Immunohistochemical study showed diffuse expression of low molecular weight cytokeratin, chromogranin A and synaptophysin, and more than 20% of the tumor cells were Ki-67 positive. Glycogen granules were found in their cytoplasm. There were clearly seen metastatic calcifications in the intramural coronary vessels, the cardiomyocytes, the kidneys and the lungs. The present case report contributes considerably to the differential diagnosis of hypercalcemia.

High prevalence of intramural coronary infection in patients with drug-resistant cardiac syndrome X: comparison with chronic stable angina and normal controls

BackgroundCoronary microvascular dysfunction has been reported along with myocardial viral infection. Whether intramural coronary vessels infection plays a role in patients with cardiac syndrome X (CSX) is unknown.MethodsThirteen consecutive patients...

Estrogen replacement therapy reverses changes in intramural coronary resistance arteries caused by female sex hormone depletion.

We tested the hypothesis that female sex hormone depletion and estradiol replacement therapy significantly influences the biomechanical properties of intramural coronary resistance arteries. Female rats (n=30) were divided into three groups. In group O, rats were subjected to bilateral ovariectomy. Group HRT was subjected to bilateral ovariectomy and estradiol replacement therapy. Rats in group C served as controls. One month after ovariectomy, intramural coronary arteries (approximately 200 microm in diameter) branching from the left anterior descending coronary were isolated, cannulated and studied by microarteriography. Intraluminal pressure was increased in steps between 0 and 90 mm Hg. The steady state diameter at each step was measured. These measurements were repeated in the presence of U46619, a thromboxane (TX) A2 receptor agonist (at a concentration of 10(-6) M), and bradykinin (BK; at 10(-6) M). Finally, Ca2+-free Krebs-induced passive diameter (PD) was measured in each group. Ovariectomy increased spontaneous myogenic tone of coronary arteries (p<0.05), which was normalized by estrogen replacement. Ovariectomy decreased distensibility observed at low pressure, although passive diameter was not changed. Estrogen replacement decreased wall stress and elastic modulus (p<0.05). The thromboxane A2 agonist induced the largest contraction in the ovariectomized group, whereas bradykinin-induced relaxation was the largest in the estrogen replacement group (p<0.05). Estradiol hormone replacement therapy (HRT) may exert a beneficial effect on myocardial perfusion in menopause by opposing the deterioration of biomechanical properties of intramural coronary resistance vessels induced by female sex hormone depletion.

Role of K(+)(ATP) channels and adenosine in regulation of coronary blood flow in the hypertrophied left ventricle.

In the hypertrophied heart, increased extravascular forces acting to compress the intramural coronary vessels might require augmentation of metabolic vasodilator mechanisms to maintain adequate coronary blood flow. Vascular smooth muscle ATP-sensitive potassium (K(+)(ATP)) channel activity is important in metabolic coronary vasodilation, and adenosine contributes to resistance vessel dilation in the hypoperfused heart. Consequently, this study was performed to determine whether K(+)(ATP) channels and adenosine have increased importance in exercise-induced coronary vasodilation in the hypertrophied left ventricle. Studies were performed in dogs in which banding of the ascending aorta had resulted in a 66% increase in left ventricular mass in comparison with historic normal animals. Treadmill exercise resulted in increases of coronary blood flow that were linearly related to the increase of heart rate or rate-pressure product. During resting conditions, K(+)(ATP) channel blockade with glibenclamide caused a 17 +/- 5% decrease in coronary blood flow, similar to that previously observed in normal hearts. Unlike normal hearts, however, glibenclamide blunted the increase in coronary flow that occurred during exercise, causing a significant decrease in the slope of the relationship between coronary flow and the rate-pressure product. Adenosine receptor blockade with 8-phenyltheophylline did not alter coronary blood flow at rest or during exercise. Furthermore, even after K(+)(ATP) channel blockade with glibenclamide, the addition of 8-phenyltheophylline had no effect on coronary blood flow. This finding was different from normal hearts, in which the addition of adenosine receptor blockade after glibenclamide impaired exercise-induced coronary vasodilation. The data suggest that, in comparison with normal hearts, hypertrophied hearts have increased reliance on opening of K(+)(ATP) channels to augment coronary flow during exercise. Contrary to the initial hypothesis, however, adenosine was not mandatory for exercise-induced coronary vasodilation in the hypertrophied hearts either during control conditions or when K(+)(ATP) channel activity was blocked with glibenclamide.

Histological evidence of concomitant intramyocardial and epicardial vasculitis in necropsied heart allografts: a possible relationship with graft coronary arteriosclerosis.

The significance of medial lymphocytic vasculitis in intramural coronary vessels in heart transplantation is very poorly understood. This study was designed to identify histological evidence of an association between the presence of epicardial coronary lesions and the occurrence of intramyocardial vasculitis and/or myocardial ischemia. We analyzed the frequency of medial vasculitis and other myocardial histological alterations in a retrospective study of 24 human cardiac allografts from patients who died of ischemic heart disease and/or myocardial rejection. Medial lymphocytic vasculitis in the myocardium was associated with vasculitis in the vasa vasorum of the epicardial coronary arteries and the presence of microfoci of acute myocardial infarction but was independent of the occurrence of myocardial fiber rejection. Chronic graft epicardial arteriopathy revealed two patterns of lesions. One pattern was similar to that of usual atherosclerosis, compromising mainly the proximal segments of the coronary artery, and was not associated with intramural vasculitis. The other pattern demonstrated diffuse involvement of the epicardial artery associated with vasculitis of its vasa vasorum and lymphocytic vasculitis of the intramural vessels. This second type of epicardial coronary lesion seemed to evolve to fibrotic arteries with thinned walls, frequently demonstrating aneurysmal dilatation with severe fibrosis of the adventitia and poor vasa vasorum. Medial vasculitis affecting intramyocardial vessels is associated with adventitial epicardial coronary vasculitis in the transplanted heart. The process of vasculitis may be involved in the development of chronic graft arteriosclerosis and is associated with ischemic myocardial lesions, but seems independent of myocardial fiber rejection.

Branching patterns of intramural coronary vessels determined by microangiography using synchrotron radiation.

The intramural coronary artery (IMCA) with a diameter of 50-500 micrometers is critical for blood supply to the inner layers of heart muscle. We introduced digital measurement to microangiography using monochromatic synchrotron radiation and quantified branching patterns of the IMCA, the epicardial coronary artery (EPCA), and the distal ileal artery (DIA). The pre- and postbranching diameters were measured (95-1,275 micrometers) in seven dogs. A typical arterial segment divided into two nearly equivalent branches, and a regression line of daughter-to-mother diameter plots was almost identical among the EPCA (y = 0.838x - 16.7 in micrometers), IMCA (y = 0.737x - 2.18), and DIA (y = 0.755x + 8.63). However, a considerable difference was present at a segment where a proximal IMCA branched off from an EPCA (y = 0.182x + 90.2). Moreover, a proximal IMCA diameter had no relationship to the branching order from an EPCA. The precision of this method was confirmed by the good correlation of diameter measurements between two independent observers (r = 0.999, y = 1.02x - 1.07). In conclusion, using digital microangiography we demonstrated that the self-similar branching pattern of coronary arteries was discrete at the connection between the IMCA and EPCA.

Desmin myopathy involving cardiac, skeletal, and vascular smooth muscle: Report of a case with immunoelectron microscopy

Desmin myopathy is a rare idiopathic disorder characterized by abnormal aggregates of desmin-type intermediate filaments, which affects cardiac and skeletal muscle, and rarely the intestinal smooth muscle. We report a 42-year-old woman with atrial fibrillation and progressive restrictive cardiomyopathy. Left ventricular biopsy, cardiac explant, and subsequent autopsy study of skeletal muscle revealed cytoplasmic granulo-filamentous inclusions that were continuous with Z-lines and were immunoreactive for desmin filaments both at the light immunohistochemical and electron microscopic level. In addition, we report the presence of characteristic inclusions within the smooth muscle of intramural coronary blood vessels. This is the first description of desmin inclusions within vascular smooth muscle, and underscores the systemic nature of this rare myopathy.

Imaging of the distal left anterior descending coronary artery by transthoracic color-doppler echocardiography

Two-dimensional echocardiography evaluates the effect of myocardial ischemia on left ventricular wall motion, but a direct measure of coronary flow by this method is still lacking. The aim of the present study is to evaluate the efficacy of new, high-resolution ultrasound equipment designed to image by color Doppler transthoracic echocardiography the epicardial and intramural coronary vessels. We have studied 33 consecutive patients in apical projections, to detect by color Doppler ≥1 segments of the middle-distal tract of the left anterior descending coronary artery. In 25 of 33 patients (76%), the middle-distal tract of the left anterior descending coronary artery was imaged by color Doppler. In 15 of 33 patients (46%), the periapical tract of the left anterior descending was imaged along with its perforating branches. In 2 of 4 patients who had coronary artery bypass grafting, the anastomosis between the left internal mammary artery and the left anterior descending coronary artery was imaged. Once the coronary artery was imaged, pulsed Doppler was used to measure coronary blood flow velocity at rest. Peak and mean flow velocity, as well as the deceleration time (msec) and deceleration rate (cm/sec 2), were measured on the diastolic phase of the Doppler tracing. In all 25 patients, it was possible to measure by pulsed Doppler the coronary flow velocity pattern characterized by a typical prevalent diastolic component. Peak diastolic flow velocity was 50 ± 17 cm/sec and mean diastolic flow velocity was 37 ± 12 cm/sec. The deceleration time was 916.2 ± 429.1 msec and the deceleration rate was 86.3 ± 69.3 cm/sec 2. The Doppler pattern of the grafted mammary artery was different from the native mammary flow. This new noninvasive imaging technique of the coronary arteries promises to expand the field of diagnostic and experimental echocardiography and brings new insight into the pathophysiology of ischemic heart disease.

Pressure-flow relations in coronary circulation

The blood vessels that run on the surface of the heart and through its muscle are compliant tubes that can be affected by the pressures external to them in at least two ways. If the pressure outside these vessels is higher than the pressure at their downstream ends, the vessels may collapse and become Starling resistors or vascular waterfalls. If this happens, the flow through these vessels depends on their resistance and the pressure drop from their inflow to the pressure around them and is independent of the actual downstream pressure. In the first part of this review, the physics of collapsible tubes is described, and the possible occurrences of vascular waterfalls in the body is evaluated. There is good evidence that waterfall behavior is seen in collateral coronary arteries and in extramural coronary veins, but the evidence that intramural coronary vessels act like vascular waterfalls is inconclusive. There is no doubt that in systole there are high tissue pressures around the intramyocardial vessels, particularly in the subendocardial muscle of the left ventricle. The exact nature and values of the forces that act at the surface of the small intramural vessels, however, are still not known. We are not certain whether radial (compressive) or circumferential and longitudinal (tensile) stresses are the major causes of vascular compression; the role of collagen struts in modifying the reaction of vessel walls to external pressures is unknown but possibly important; direct examination of small subepicardial vessels has failed to show vascular collapse. One of the arguments in favor of intramyocardial vascular waterfalls has been that during a long diastole the flow in the left coronary artery decreases and reaches zero when coronary arterial pressure is still high: it can be as much as 50 mmHg in the autoregulating left coronary arterial bed and approximately 15-20 mmHg even when the vessels have been maximally dilated. These high zero flow pressures, especially during maximal vasodilatation, have been regarded as indicating a high back pressure to flow that is due to waterfall behavior of vessels that are exposed to tissue pressures.(ABSTRACT TRUNCATED AT 400 WORDS)

Intramural coronary vessels in partial absence of the myocardium of the right ventricle

Partial absence of the right ventricular (RV) myocardium characterized by its replacement by adipose tissue, also known as RV displasia and RV myocardiopathy, has been reported in many patients. They are usually young adults with arrhythmia or sudden death 1; some cases have had progressive heart failure. 2 Recently microscopic lesions in the myocardial fibers have been demonstrated. 3 We present such a case in which we found alterations in the intramural coronary vessels that have not been described so far.

Spontaneous extramural coronary arteritis in dogs.

Control and treated beagle and random-source dog hearts obtained from 119 toxicological experiments were evaluated histologically to study the incidence and characteristics of a microscopic inflammatory lesion specific to the extramural coronary arteries. The lesion occurred in 23% of the experiments. The incidence was 2.3% of the control and treated beagle hearts examined. In the control beagles, it was present in 3.1% of males and 1.3% of females and in the treated beagles, in 1.8% males and 2.8% females. It occurred in 4.7% of the random-source animals. While not visible grossly, histologically, the solitary lesions were characterized by adventitial infiltrates of mononuclear cells, occasional areas of necrosis with inflammatory cell infiltrates occurring in the mural and subendothelial regions. The latter resulted in prominent separation of the intima from the media. The lesions occurred in the right and left coronary arteries and in the dorsal, circumflex and ventral descending branches of the left coronary artery. Similar vascular lesions were not found in the intramural coronary vessels or in other organs in the affected animals. Expanded sampling of the extramural coronary arteries revealed an incidence of 5-9%. This lesion of focal extramural coronary arteritis was considered idiopathic, and not a manifestation of recently reported polyarteritis syndromes in dogs.

Idiopathic extramural coronary arteritis in beagle and mongrel dogs.

Hearts obtained from 119 toxicological experiments on dogs during a 21-year period (1965-1986) were evaluated histologically to determine the incidence and characteristics of focal microscopic inflammatory lesions of the extramural coronary arteries. Lesions were encountered in 23% of 119 experiments. The average overall incidence was 2.3% of 1,905 control and chemically treated male and female beagle hearts (3.1% of male and 1.3% of female control beagles, and 1.8% of male and 2.8% of female treated beagles). Lesions were seen in 4.7% of 127 random-source mongrel dogs. Histologically, lesions were characterized by adventitial infiltrates of mononuclear cells, areas of mural necrosis, and inflammatory cell infiltrates in both mural and subendothelial regions. In the latter region, fibrosis developed separating the intima from the internal elastic membrane. Lesions occurred in the right and left coronary arteries and in the dorsal, circumflex, and ventral descending branches of the left coronary artery. Vascular lesions were not present in the intramural coronary vessels or in vessels of other organs in affected animals. More extensive sampling of the extramural coronary arteries revealed an incidence of 5-9%. The lesion of focal extramural coronary arteritis was idiopathic, and not a manifestation of the polyarteritis syndrome of dogs.

Effect of experimental infarct on the mortality rate in alloxan-diabetic rats

The authors report the wide mortality observed in alloxan diabetic rats infarcted with large doses of isoproterenol. The experimental data are in line with the results of clinical studies testifying that the diabetic disease involves the cardiovascular system and affects the prognosis of myocardial infarct. These experiences do not permit to define the direct mechanism(s) responsible for the high mortality in diabetic infarcted rats over controls (diabetic not infarcted); however these results give rise to a discussion on the following topics: 1. The damage of intramural coronary vessels as a cause of depressed cardiac contractility in diabetic rats. 2. The role of reduced plasmatic levels of insulin in depressing myocardial performance in alloxan diabetic rats. 3. The hyperglycaemia-provoking effect of isoproterenol as a contributing factor in the death of diabetic rats. 4. The possible direct action of diabetogenic doses of alloxan on the myocardium.

Left ventricular outflow obstruction caused by a Starr-Edwards mitral prosthesis

ranged from 400,000 to 800,000/mm3. The final hospital admission at age 22 years was necessitated by severe CHF and ischemia of the distal left fourth finger. Cardiac output and blood pressure diminished progressively and the patient died 10.5 months after the acute MI. At necropsy (Medical College of Ohio #A-82-2), the heart weighed 450 g. The apical half of the anterior LV free wall was replaced by dense scar at and adjacent to the LV aneurysectomy incision (Fig. I). The posterior LV wall was also scarred. The LV apex contained mural thrombus adherent to underlying endocardial fibrous tissue. Fresh and organized mural thrombus also covered the LV outflow tract (Fig. 2). The R and LAD were totally occluded proximally; the length of the LAD occlusion was approximately 2 cm and that of the R 4 cm. The other portions of the LAD and R and the entire left circumflex artery were normal. Branches of the major epicardial coronary contained discrete focal severe narrowings with normal intervening areas. Histologic examination of the narrowed coronary arterial segments showed fibrocellular intimal profileration without foam cells, cholesterol clefts, pultaceous debris or calcific deposits (Fig. 3). In some segments, the lumen contained several small channels, and a platelet-fibrin thrombus was present in the LAD (Fig. 3). The intima of the narrowed coronary arteries was similar histologically to the thickened fibrous tissue on the LV mural endocardium (Fig. 4). Histologic examination of LV myocardium disclosed necrosis adjacent to the healed MI and multiple small intramural coronary vessels with plateletfibrin thromboemboli (Fig. 4). Both the spleen and lung contained discrete infarcts. The aorta was free of atherosclerotic plaques. The bone marrow, specifically the megakaryocytes, was normals The kidneys contained focal hyaline sclerosis of glomerular capillary tufts consistent with organized microthrombi, but no other abnormalities to explain the hematuria and proteinuria throughout childhood. (Sections of kidney were examined by John M. Kissane, MD, a recognized renal expert, who agreed with our renal diagnosis.)

Sekundäre kongestive Kardiomyopathie nach Adriamycin*

Doxorubicin at a dose of 470 mg/m2 body surface, was administered to a 15-year-old boy with metastasising osteosarcoma. The cumulative dose caused severe "secondary congestive cardiomyopathy", which ended fatally, although the cumulative dose was below the recommended limit of 550 mg/m2. No other treatment for the tumour had been given. Postmortem examination revealed obliterative lesions in the intramural coronary vessels and electron-microscopy showed all the features of a cardiomyopathy at cellular level.