Mortality statistics from multicenter studies outlined some high risk characteristics of patients with coronary heart disease subjected to coronary angiography. Among these, the left main disease carries the worst prognosis. The features of left main disease patients with a higher mortality probability during coronary angiography are described. Data were collected prospectively on 4844 patients subjected to coronary angiography. No death was recorded in patients without left main disease (4641 patients) independently of other risk factors: number of diseased vessels, NYHA status, clinical picture, or ejection fraction. From the 203 patients with left main disease, 30 had a left ostial lesion (14% of the patients with left main disease). The three patients who died during the procedure were among those with left ostial lesion. Therefore, despite the fact that the incidence of mortality in all patients in general who are subjected to coronary angiography was small (0.06%) there was a subgroup of patients with ostial lesion who carried high mortality (10%) (p < 0.0009).
Ventricular diverticula are rare abnormalities of the heart, whose origin is not fully understood yet. They are mostly congenital, either isolated or associated with other cardiac and extracardiac defects (Cantrell’s pentalogy). Although their etiology is not clear, an embryologic developmental defect has been proposed. Yet, some of them are associated with cardiomyopathies, inflammation or trauma. We discuss the case of a patient with hypertrophic cardiomyopathy and an apical diverticulum. The hypothesis made was that, an obstructing hypertrophic mass, localized in the midportion of the left ventricle, creates a pressure gradient between the apical and basal portions which finally leads to the creation of the diverticulum. Acute rupture, ventricular arrhythmias, peripheral arterial embolism and infective endocarditis are few of their complications. Besides transthoracic 2-D echocardiography and left ventriculography, magnetic resonance imaging (MRI) is the gold standard means of diagnosis. The opinions in the literature, as far as the pharmacological treatment or surgical resection, are controversial.
Left ventricular aneurysms (LVAs) can be congenital or acquired. They develop most frequently after myocardial infarction. Other causes include hypertrophic cardiomyopathy, arrythmogenic right ventricular cardiomyopathy, myocarditis, chest trauma, sarcoidosis or Chagas disease [1, 2]. LVAs without identifiable cause are considered as idiopathic. Most of LVAs are asymptomatic and are occasionally identified during routine diagnostic procedures. However, in rare cases LVAs may be associated with life-threatening ventricular tachyarrhythmias (mostly ventricular tachycardia, VT) and sudden cardiac death, even as a first manifestation [3]. In most of the cases VT has right bundle branch block morphology consistent with left ventricular origin. Idiopathic LVAs are anatomically distinguished from congenital diverticula, which are characterized by a narrow communication with the ventricle [2, 4].
In this report we describe an interesting and rare case of idiopathic LVA associated with sustained monomorphic VT, ventriculoatrial conduction and intermittent Wenckebach block. Management strategies are discussed and our treatment approach is presented.
Case Report
A 72-year old woman was admitted to our hospital with palpitations, dizziness and fatigue from a few hours ago. The patient had a history of heart failure (NYHA II) from three years ago and also an episode of paroxysmal atrial flutter two years ago. She was free of angina and had no cardiovascular disease risk factors. The family history was unremarkable with respect to cardiac arrest, unexplained syncope, ventricular tachyarrhythmias, or cardiomyopathy. At the time of presentation to the emergency department the patient was receiving carvedilol, valsartan, and furosemide. The baseline 12-lead ECG revealed a sustained monomorphic VT with RBBB morphology and left axis deviation (Fig. 1A1A). Since tachycardia was poorly tolerated with systolic blood pressure of 80 mmHg an electrical cardioversion was applied and the rhythm was restored to sinus (Fig. 1B1B). The ECG, physical examination and laboratory tests after the cardioversion were unremarkable.
Fig. (1A)
ECG on admission showing the ventriculat tachycardia (VT) with RBBB morphology, (B). Restoration of VT to sinus rhythm with electrical cardioversion, (C). Induced VT with LBBB morphology during the electrophysiology study, (D). Electrogram during the ...
The chest X-ray revealed an increased cardiothoracic index. The transthoracic echocardiogram showed dilated left ventricle with a lateral wall aneurysm, left ventricular ejection fraction of 40% and mild mitral regurgitation (Fig. 2A2A). The coronary angiography revealed normal coronary arteries, whereas the left ventriculography further confirmed the lateral wall aneurysm (Fig. 2B2B). Magnetic resonance imaging further confirmed the presence of the LVA (Fig. 2C2C).
Fig. (2A)
Echocardiogram showing the left ventricular aneurysm (arrows), (B). Left ventriculography further depicting the lateral wall aneurysm (arrows), (C). Magnetic resonance imaging further confirmed the presence of an aneurysm with wall thinning (arrows).
The patient was started on amiodarone per os and after two weeks an electrophysiology study was performed. The programmed ventricular stimulation in the right ventricular apex with 500/230-240 msec basic drive cycle and two extrastimuli reproducibly induced sustained monomorphic VT of 160 bpm associated with hemodynamic instability. That tachycardia, however, had different characteristics from the one at the emergency department as it was associated with left branch bundle block (LBBB) morphology and normal cardiac axis and was terminated by overdrive pacing (Fig. 1C1C). The LBBB morphology was consistent with septal origin of the VT. Of note, during the inducible VT a 1:1 ventriculoatrial conduction with intermittent Wenckebach block was recorded (Fig. 1D1D). A cardioverter defibrillator (ICD) was implanted for the secondary prevention of VT and the patient was discharged 2 days after ICD implantation on treatment with carvedilol, amiodarone and angiotensin converting enzyme inhibitor. During a follow-up period of six months no ventricular arrhythmias occurred.
Cardiac resynchronization therapy (CRT) is a new therapy that improves hemodynamics and symptroms in patients with advanced heart failure by restoring more synchronized contraction patterns.
Spontaneous coronary artery dissection is a rare cause of acute ischemic coronary events and sudden cardiac death. It usually occurs in young women without traditional risk factors for coronary artery disease during pregnancy or postpartum period. However, it has also been reported in patients with atherosclerotic coronary disease. We present a case of spontaneous right coronary artery dissection in a 48-year male with recent myocardial infarction and previous percutaneous coronary intervention.
Left ventricular dyssynchrony is an independent predictor for adverse cardiac events. Resynchronization therapy improves inter-and intraventricular dyssynchrony in patients with dilated hearts and intraventricular conduction delays.Tissue doppler imaging (TDI) is the only method able to detect regional myocardial asynchrony. Our purposeis to assess the impact of biventricular pacing on inter-and intraventricular asynchrony. Fourteen patients with advanced heart failure (NYHA class >= III), EF< 35%,QRS 165±15 msec, were studied before and 24 hours after implantation of a CRT system. Heart rate(HR),QRSduration,electromechanical coupling time for the left(Qaorta) and right ventricle(Qpulm) and their difference (Qpulm-Qaort) were calculated before and the day after implantation of a biventricular pacemaker.Tissue doppler velocities and timings (from the onset of the QRS complex to peak systole) were measured in 2 basal and 2 middle segments for longitudinal function(4C apical view).We calculated and compared the changes for both modalities(off and CRT-on). Statistical analysis was performed with the Wilcoxon Matched Pairs Test. CRT improves inter- and intraventricular asynchrony. Tissue velocity imaging revealed significant restoration of synchronous contraction in the basal parts of the left ventricle after CRT
