Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Age | Gender | Occupation | Working Diagnosis |
---|---|---|---|
54 Years | Male | Business Entrepreneur | Non-ischemic idiopathic cardiomyopathy |
This 54-year-old man first sought treatment in 2005 with symptoms of progressive dyspnea on exertion, pedal edema accompanied by paroxysmal nocturnal dyspnea, and orthopnea. He had initially been treated in the community for upper respiratory tract infection with oral antibiotics but then developed symptoms of shortness of breath and fatigue. On further medical testing, he was diagnosed with dilated cardiomyopathy. His initial echocardiogram showed dilated cardiomyopathy with left ventricular internal diameter at end-diastole of 64 mm Hg, left ventricular ejection fraction (LVEF) of 18% with diffuse hypokinesis, moderate mitral regurgitation, left atrial enlargement, and moderate-to-severe tricuspid regurgitation.
The patient’s risk factors included active cigarette smoking, with a 25 pack-year history, and hyperlipidemia. He underwent cardiac catheterization, which showed mild obstructive coronary artery disease; however, this was unlikely to explain the severity of his cardiomyopathy and symptoms.
A single-lead implantable cardioverter-defibrillator (ICD) was originally placed in March 2010 for New York Heart Association (NYHA) class II symptoms with a QRS duration of 110 ms. Progressive worsening and widening of his QRS duration resulted in an upgrade to a cardiac resynchronization therapy defibrillator (CRT-D) with the addition of atrial and left ventricular leads. His NYHA classification had worsened to NYHA class III with hospitalizations for heart failure. Because of his relatively narrow QRS duration (126 ms), he also underwent a dyssynchrony echocardiographic study to ascertain the potential value of an upgrade of his ICD.
After the upgrade he came to our clinic for an unscheduled visit after being “bothered” by an audible tone from his device occurring every morning over several consecutive days. He described it as “an annoying occurrence” during his morning business meetings. His device interrogation was notable for inappropriate ICD therapy having occurred while he was asleep 7 days previously. The intracardiac electrograms documented atrial fibrillation with rapid ventricular response, which converted to sinus rhythm after he received one 34-J shock. After this initial shock he connected and established himself on our remote monitoring system.
He proceeded over the next several months to have several episodes of paroxysmal atrial fibrillation, which were detected accurately by his remote monitoring intracardiac electrograms, as exemplified in Table 48-1 . Amiodarone therapy was started, but poorly tolerated secondary to neurologic effects of increased somnolence and fatigue, which led to the patient discontinuing the medication. On the amiodarone, his activity level decreased significantly, as seen on remote monitoring, although his biventricular pacing quantities went up significantly, as highlighted and circled in Figure 48-1 .
Type | ATP Seq | Shocks | Success | ID no. | Date | Time hh:mm | Duration hh:mm:ss |
Av erage BPM A/V |
---|---|---|---|---|---|---|---|---|
AT/AF | 102 | 17-Sep-2012 | 04:32 | (Episode in progress) | ||||
AT/AF | 101 | 17-Sep-2012 | 03:48 | :44:22 | 178/98 | |||
AT/AF | 100 | 17-Sep-2012 | 00:16 | 03:31:53 | 180/90 | |||
AT/AF | 99 | 16-Sep-2012 | 02:17 | 21:58:27 | 180/91 | |||
AT/AF | 98 | 15-Sep-2012 | 23:20 | 02:57:42 | 178/89 | |||
AT/AF | 97 | 15-Sep-2012 | 01:10 | 22:09:17 | 180/90 | |||
AT/AF | 96 | 15-Sep-2012 | 00:06 | 01:04:13 | 175/87 | |||
AT/AF | 95 | 14-Sep-2012 | 14:10 | 09:56:19 | 178/88 | |||
AT/AF | 94 | 14-Sep-2012 | 13:59 | :10:43 | 176/88 | |||
AT/AF | 93 | 14-Sep-2012 | 08:20 | 05:38:34 | 176/88 | |||
AT/AF | 92 | 14-Sep-2012 | 05:22 | 02:57:52 | 176/86 | |||
AT/AF | 91 | 13-Sep-2012 | 19:38 | 09:44:24 | 169/83 |
The choices for alert alarms are audible and/or system monitor alerts that can range from 3 to 24 hours, including settings for the accompanying ventricular rates. For patients with heart failure, it is beneficial to set these parameters conservatively because the onset of atrial fibrillation could exacerbate their heart failure.
As a result of increasing heart failure symptoms, a month-long trial of turning off the left ventricular lead was done, but his heart failure symptoms worsened over the following weeks. As indicated earlier, his baseline QRS duration was fairly narrow, at 126 ms, which can be a substrate for nonresponse to CRT.
As his heart failure progressed, he developed multiple episodes of nonsustained ventricular tachycardia, some of which occurred at ventricular rates as low as 131 bpm. These ventricular arrhythmias were preceded by elevations in his intrathoracic lead impedance fluid index trends measured in Ohms and identified as OptiVol in Medtronic (Medtronic, Minneapolis, Minn.) devices. His impedance measurements became important to monitor on a regular basis, because they were an accurate predictor of his heart failure exacerbations. Remote monitoring trends of these episodes are viewed in Figure 48-2 .
The patient’s clinical trajectory went further downhill as he developed persistent atrial fibrillation, with rapid ventricular rates and decreased percentages of biventricular pacing ultimately requiring cardioversion. Because of the size of his left atrium, the occurrence of atrial fibrillation was not unexpected. He had not been on anticoagulation therapy and was started on dabigatran when his lifestyle proved that he would not be compliant for frequent blood level international normalized ratio blood sample checks on warfarin.
The patient was taking captopril 6.25 mg three times daily, carvedilol 6.25 mg twice daily, furosemide 40 mg twice daily, spironolactone 25 mg daily, digoxin 0.125 mg daily, atorvastatin 80 mg daily, and aspirin 81 mg daily. Carvedilol was discontinued when his blood pressure was no longer high enough, and metoprolol was resumed. His diuretic medications included torsemide 80 mg twice daily, with an additional 80 mg as needed based on daily weight. Metolazone 2.5 mg was then added on an as-needed basis. His intolerance of amiodarone and ongoing ventricular arrhythmias necessitated the initiation of low-dose sotalol, which was eventually titrated up to 120 mg twice daily for treatment of ventricular arrhythmias as documented by his remote transmission ( Figure 48-3 ) that required ICD therapies.
The remote monitoring of cardiac implantable devices is rapidly growing throughout most of our clinical practices. Remote transmissions are being used to replace in-office device checks and provide a method of surveillance for recalled leads. For patients with CRT devices, programmed device alerts are frequently indicative of a clinical change requiring intervention. Previous work reported that 86% of remote monitoring events done on daily transmissions were due to medical conditions, including detection of supraventricular or ventricular arrhythmias, ICD therapy, or paroxysmal atrial fibrillation, as opposed to lead or technical problems. Early detection of these electrophysiologic issues or clinical trends can result in earlier intervention and decreased mortality. In this case study, close monitoring of the patient alerts through the remote system prevented several potential admissions and ICD therapies because his medications were adjusted while he remained at home. In this single case study the audible alert actually prompted the patient’s first clinic visit. He sought health care only because of the bothersome audible tone coming from his device. This may serve as a useful feature to keep programmed on in patients with issues of compliance. The Diagnostic Outcome Trial in Heart Failure (DOT-HF) study demonstrated that audible alerts may increase hospital admissions. This is because OptiVol measures as a predictor of heart failure exacerbations lack specificity and may result in patients and physicians overreacting to a false-positive alert.
BP/HR: 120/70 mm Hg/80 bpm
Height/weight: 97.5 kg/182.9 cm
Body mass index: 29.2
Head, ears, eyes, nose, throat: Unremarkable
Neck: Supple; positive jugular venous distention up to 9 cm without carotid bruits
Lungs: Scattered crackles were present bilaterally
Heart: Regular rate and rhythm, normal first heart sound (S 1 ) and second heart sound (S 2 ), no murmurs or gallops
Abdomen: Soft, nontender, with no organomegaly
Extremities: Trace edema present laterally, with 2+ distal pulses
Hemaglobin: 9.3 g/dL
Hematocrit/packed cell volume: 29.3%
Platelet count: 195 × 10 3 /µL
Sodium: 122 mmol/L
Potassium: 4.3 mmol/L
Creatinine: 3.2-4.8 mmol/L
Blood urea nitrogen: 39-72 mg/dL
The electrocardiogram showed sinus rhythm at 67 bpm, first-degree atrioventricular block with a PR interval of 228 ms, QRS duration 126 ms, left axis deviation consistent with a left anterior fascicular hemiblock, poor R-wave progression across the precordium, and Q-waves in the inferior leads.
On chest radiography the cardiomyopathy was shown to be stable. Both lungs were inflated and clear ( Figure 48-4 ).
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here